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Attacking Cancer Progression and Metastasis
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Attacking Cancer Progression and Metastasis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 59134

Special Issue Editor

Dr. Luba Hunáková

E-Mail Website
Guest Editor
Faculty of Medicine, Comenius University in Bratislava, Sasinkova 4, 81713108 Bratislava, Slovakia
Interests: Apoptosis; Flow cytometry; Breast cancer; Immune system; Tumor microenvironment; Neurobiology; Cancer survivorship; cytotoxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer metastasis is the leading cause of cancer-related deaths. In spite of progress in the survival of cancer patients, there is an urgent need to understand the mechanisms of cancer progression for the development of novel preventive and therapeutic approaches for controlling its spread.

This Special Issue is focused on the collection of papers on “Attacking cancer progression and metastasis”. It provides an effective way to communicate current knowledge about the cellular and molecular mechanisms involved in cancer progression and metastasis and/or to suggest new targets for possible future therapeutic interventions. It is aimed at giving ample scope for new ideas about how to block or weaken processes of cancer’s progression to its final stage.

In the current series, we invite papers from basic research, translational research, and clinical studies on all aspects of possible targetable mechanisms leading to effective interventions in the future.

Dr. Luba Hunáková
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer progression
  • metastasis
  • molecular mechanisms
  • drugs
  • exosomes
  • EMT
  • angiogenesis
  • cytotoxicity
  • mi-RNA
  • tumor microenvironment
  • stem cells

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Published Papers (17 papers)

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Editorial

Jump to: Research, Review

3 pages, 189 KiB  
Editorial
Attacking Cancer Progression and Metastasis
by Ľuba Hunáková
Int. J. Mol. Sci. 2023, 24(9), 7858; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24097858 - 26 Apr 2023
Viewed by 870
Abstract
This Special Issue, focused on a collection of papers on “attacking cancer progression and metastasis”, is devoted to communicating current knowledge about the cellular and molecular mechanisms involved in cancer progression and metastasis, as well as suggesting new targets for possible future therapeutic [...] Read more.
This Special Issue, focused on a collection of papers on “attacking cancer progression and metastasis”, is devoted to communicating current knowledge about the cellular and molecular mechanisms involved in cancer progression and metastasis, as well as suggesting new targets for possible future therapeutic interventions [...] Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)

Research

Jump to: Editorial, Review

13 pages, 2236 KiB  
Article
Anti-Stem Cell Property of Pterostilbene in Gastrointestinal Cancer Cells
by Shiori Mori, Shingo Kishi, Kanya Honoki, Rina Fujiwara-Tani, Takuma Moriguchi, Takamitsu Sasaki, Kiyomu Fujii, Shinji Tsukamoto, Hiromasa Fujii, Akira Kido, Yasuhito Tanaka, Yi Luo and Hiroki Kuniyasu
Int. J. Mol. Sci. 2020, 21(24), 9347; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249347 - 08 Dec 2020
Cited by 15 | Viewed by 2480
Abstract
Pterostilbene (PTE) is a natural sterbenoid contained in blueberries that has an antioxidant effect. In contrast, PTE also generates oxidative stress in cancer cells and provides an antitumor effect. Here, we examined the potential mechanism of this contrasting effect of PTE using three [...] Read more.
Pterostilbene (PTE) is a natural sterbenoid contained in blueberries that has an antioxidant effect. In contrast, PTE also generates oxidative stress in cancer cells and provides an antitumor effect. Here, we examined the potential mechanism of this contrasting effect of PTE using three gastrointestinal cancer cell lines, namely CT26, HT29, and MKN74. PTE showed a dose-dependent inhibition of cell proliferation, sphere-forming ability, and stem cell marker expression in all three cell lines. Furthermore, the cells treated with PTE showed an increase in mitochondrial membrane potential and an increase in mitochondrial oxidative stress and lipid peroxide. Upon concurrent treatment with vitamin E, N-acetyl-L-cysteine, and PTE, the PTE-induced mitochondrial oxidative stress and growth inhibition were suppressed. These findings indicate that PTE induces oxidative stress in cancer cells, suppresses stemness, and inhibits proliferation. These antitumor effects of PTE are considered to be useful in cancer treatment. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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22 pages, 2320 KiB  
Article
Impairment of Hypoxia-Induced CA IX by Beta-Blocker Propranolol—Impact on Progression and Metastatic Potential of Colorectal Cancer Cells
by Monika Barathova, Katarina Grossmannova, Petra Belvoncikova, Veronika Kubasova, Veronika Simko, Rudolf Skubla, Lucia Csaderova and Jaromir Pastorek
Int. J. Mol. Sci. 2020, 21(22), 8760; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228760 - 19 Nov 2020
Cited by 14 | Viewed by 2561
Abstract
The coexistence of cancer and other concomitant diseases is very frequent and has substantial implications for treatment decisions and outcomes. Beta-blockers, agents that block the beta-adrenergic receptors, have been related also to cancers. In the model of multicellular spheroids formed by colorectal cancer [...] Read more.
The coexistence of cancer and other concomitant diseases is very frequent and has substantial implications for treatment decisions and outcomes. Beta-blockers, agents that block the beta-adrenergic receptors, have been related also to cancers. In the model of multicellular spheroids formed by colorectal cancer cells we described a crosstalk between beta-blockade by propranolol and tumour microenvironment. Non-selective beta-blocker propranolol decreased ability of tumour cells to adapt to hypoxia by reducing levels of HIF1α and carbonic anhydrase IX in 3D spheroids. We indicated a double action of propranolol in the tumour microenvironment by inhibiting the stability of HIF1α, thus mediating decrease of CA IX expression and, at the same time, by its possible effect on CA IX activity by decreasing the activity of protein kinase A (PKA). Moreover, the inhibition of β-adrenoreceptors by propranolol enhanced apoptosis, decreased number of mitochondria and lowered the amount of proteins involved in oxidative phosphorylation (V-ATP5A, IV-COX2, III-UQCRC2, II-SDHB, I-NDUFB8). Propranolol reduced metastatic potential, viability and proliferation of colorectal cancer cells cultivated in multicellular spheroids. To choose the right treatment strategy, it is extremely important to know how the treatment of concomitant diseases affects the superior microenvironment that is directly related to the efficiency of anti-cancer therapy Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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13 pages, 5925 KiB  
Article
MYC Targets Scores Are Associated with Cancer Aggressiveness and Poor Survival in ER-Positive Primary and Metastatic Breast Cancer
by Amy Schulze, Masanori Oshi, Itaru Endo and Kazuaki Takabe
Int. J. Mol. Sci. 2020, 21(21), 8127; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218127 - 30 Oct 2020
Cited by 66 | Viewed by 3779
Abstract
MYC is one of the most studied oncogenes that is known to promote cell proliferation. We utilized MYC targets v1 and MYC targets v2 scores of gene set variation analysis and hypothesized that these scores correlate with tumor aggressiveness and survival outcomes. We [...] Read more.
MYC is one of the most studied oncogenes that is known to promote cell proliferation. We utilized MYC targets v1 and MYC targets v2 scores of gene set variation analysis and hypothesized that these scores correlate with tumor aggressiveness and survival outcomes. We examined a total of 3109 breast cancer patients from TCGA, METABRIC, and GSE124647 cohorts. In each cohort, the patients were divided into high- and low-score groups using the upper third value as the cut off. As expected, higher scores were related to increased cell proliferation and worse clinical and pathologic features. High MYC targets scores were associated with worse survival, specifically in primary ER-positive breast cancer, consistently in both TCGA and METABRIC cohorts. In ER-positive breast cancer, high MYC targets v1, but not v2 score, was associated with high mutation load, and high MYC targets v1 and v2 scores were both associated with increased infiltration of pro- and anti-cancerous immune cells. We found that high MYC scores were associated with worse survival in metastatic breast cancer. Our findings show that the MYC targets v1 and v2 scores are associated with tumor aggressiveness and poor prognosis in ER-positive primary tumors, as well as in metastatic breast cancer. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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19 pages, 3062 KiB  
Article
RAGE Up-Regulation Differently Affects Cell Proliferation and Migration in Pancreatic Cancer Cells
by Priyanka Swami, Swetha Thiyagarajan, Arianna Vidger, Venkata S. K. Indurthi, Stefan W. Vetter and Estelle Leclerc
Int. J. Mol. Sci. 2020, 21(20), 7723; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207723 - 19 Oct 2020
Cited by 14 | Viewed by 3017
Abstract
The receptor for advanced glycation end products (RAGE) contributes to many cellular aspects of pancreatic cancer including cell proliferation, migration, and survival. Studies have shown that RAGE activation by its ligands promotes pancreatic tumor growth by stimulating both cell proliferation and migration. In [...] Read more.
The receptor for advanced glycation end products (RAGE) contributes to many cellular aspects of pancreatic cancer including cell proliferation, migration, and survival. Studies have shown that RAGE activation by its ligands promotes pancreatic tumor growth by stimulating both cell proliferation and migration. In this study, we investigated the effect of RAGE up-regulation on the proliferation and migration of the human pancreatic cancer Panc-1 cell-line. We show that moderate overexpression of RAGE in Panc-1 cells results in increased cell proliferation, but decreased cell migration. The observed cellular changes were confirmed to be RAGE-specific and reversible by using RAGE-specific siRNAs and the small molecule RAGE inhibitor FPS-ZM1. At the molecular level, we show that RAGE up-regulation was associated with decreased activity of FAK, Akt, Erk1/2, and NF-κB signaling pathways and greatly reduced levels of α2 and β1 integrin expression, which is in agreement with the observed decreases in cell migration. We also demonstrate that RAGE up-regulation changes the expression of key molecular markers of epithelial-to-mesenchymal transition (EMT). Our results suggest that in the absence of stimulation by external ligands, RAGE up-regulation can differently modulate cell proliferation and migration in pancreatic cancer cells and regulates partly EMT. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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20 pages, 3422 KiB  
Article
IRF-1 Inhibits Angiogenic Activity of HPV16 E6 Oncoprotein in Cervical Cancer
by Seung Bae Rho, Seung-Hoon Lee, Hyun-Jung Byun, Boh-Ram Kim and Chang Hoon Lee
Int. J. Mol. Sci. 2020, 21(20), 7622; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207622 - 15 Oct 2020
Cited by 13 | Viewed by 2599
Abstract
HPV16 E6 oncoprotein is a member of the human papillomavirus (HPV) family that contributes to enhanced cellular proliferation and risk of cervical cancer progression via viral infection. In this study, interferon regulatory factor-1 (IRF-1) regulates cell growth inhibition and transcription factors in immune [...] Read more.
HPV16 E6 oncoprotein is a member of the human papillomavirus (HPV) family that contributes to enhanced cellular proliferation and risk of cervical cancer progression via viral infection. In this study, interferon regulatory factor-1 (IRF-1) regulates cell growth inhibition and transcription factors in immune response, and acts as an HPV16 E6-binding cellular molecule. Over-expression of HPV16 E6 elevated cell growth by attenuating IRF-1-induced apoptosis and repressing p21 and p53 expression, but activating cyclin D1 and nuclear factor kappa B (NF-κB) expression. The promoter activities of p21 and p53 were suppressed, whereas NF-κB activities were increased by HPV16 E6. Additionally, the cell viability of HPV16 E6 was diminished by IRF-1 in a dose-dependent manner. We found that HPV16 E6 activated vascular endothelial growth factor (VEGF)-induced endothelial cell migration and proliferation as well as phosphorylation of VEGFR-2 via direct interaction in vitro. HPV16 E6 exhibited potent pro-angiogenic activity and clearly enhanced the levels of hypoxia-inducible factor-1α (HIF-1α). By contrast, the loss of function of HPV16 E6 by siRNA-mediated knockdown inhibited the cellular events. These data provide direct evidence that HPV16 E6 facilitates tumour growth and angiogenesis. HPV16 E6 also activates the PI3K/mTOR signalling cascades, and IRF-1 suppresses HPV16 E6-induced tumourigenesis and angiogenesis. Collectively, these findings suggest a biological mechanism underlying the HPV16 E6-related activity in cervical tumourigenesis. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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13 pages, 3166 KiB  
Article
Develop a High-Throughput Screening Method to Identify C-P4H1 (Collagen Prolyl 4-Hydroxylase 1) Inhibitors from FDA-Approved Chemicals
by Shike Wang, Kuo-Hao Lee, Nathalia Victoria Araujo, Chang-Guo Zhan, Vivek M. Rangnekar and Ren Xu
Int. J. Mol. Sci. 2020, 21(18), 6613; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186613 - 10 Sep 2020
Cited by 3 | Viewed by 2671
Abstract
Collagen prolyl 4-hydroxylase 1 (C-P4H1) is an α-ketoglutarate (α-KG)-dependent dioxygenase that catalyzes 4-hydroxylation of proline on collagen. C-P4H1-induced prolyl hydroxylation is required for proper collagen deposition and cancer metastasis. Therefore, targeting C-P4H1 is considered a potential therapeutic strategy for collagen-related cancer progression and [...] Read more.
Collagen prolyl 4-hydroxylase 1 (C-P4H1) is an α-ketoglutarate (α-KG)-dependent dioxygenase that catalyzes 4-hydroxylation of proline on collagen. C-P4H1-induced prolyl hydroxylation is required for proper collagen deposition and cancer metastasis. Therefore, targeting C-P4H1 is considered a potential therapeutic strategy for collagen-related cancer progression and metastasis. However, no C-P4H1 inhibitors are available for clinical testing, and the high content assay is currently not available for C-P4H1 inhibitor screening. In the present study, we developed a high-throughput screening assay by quantifying succinate, a byproduct of C-P4H-catalyzed hydroxylation. C-P4H1 is the major isoform of collagen prolyl 4-hydroxylases (CP4Hs) that contributes the majority prolyl 4-hydroxylase activity. Using C-P4H1 tetramer purified from the eukaryotic expression system, we showed that the Succinate-GloTM Hydroxylase assay was more sensitive for measuring C-P4H1 activity compared with the hydroxyproline colorimetric assay. Next, we performed high-throughput screening with the FDA-approved drug library and identified several new C-P4H1 inhibitors, including Silodosin and Ticlopidine. Silodosin and Ticlopidine inhibited C-P4H1 activity in a dose-dependent manner and suppressed collagen secretion and tumor invasion in 3D tissue culture. These C-P4H1 inhibitors provide new agents to test clinical potential of targeting C-P4H1 in suppressing cancer progression and metastasis. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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17 pages, 1241 KiB  
Article
Reciprocal Dysregulation of MiR-146b and MiR-451 Contributes in Malignant Phenotype of Follicular Thyroid Tumor
by Margarita Knyazeva, Ekaterina Korobkina, Alexey Karizky, Maxim Sorokin, Anton Buzdin, Sergey Vorobyev and Anastasia Malek
Int. J. Mol. Sci. 2020, 21(17), 5950; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21175950 - 19 Aug 2020
Cited by 11 | Viewed by 2289
Abstract
Over the last few years, incidental thyroid nodules are being diagnosed with increasing frequency with the use of highly sensitive imaging techniques. The ultrasound thyroid gland examination, followed by the fine-needle aspiration cytology is the standard diagnostic approach. However, in cases of the [...] Read more.
Over the last few years, incidental thyroid nodules are being diagnosed with increasing frequency with the use of highly sensitive imaging techniques. The ultrasound thyroid gland examination, followed by the fine-needle aspiration cytology is the standard diagnostic approach. However, in cases of the follicular nature of nodules, cytological diagnosis is not enough. Analysis of miRNAs in the biopsy presents a promising approach. Increasing our knowledge of miRNA’s role in follicular carcinogenesis, and development of the appropriate the miRNA analytical technologies are required to implement miRNA-based tests in clinical practice. We used material from follicular thyroid nodes (n.84), grouped in accordance with their invasive properties. The invasion-associated miRNAs expression alterations were assayed. Expression data were confirmed by highly sensitive two-tailed RT-qPCR. Reciprocally dysregulated miRNAs pair concentration ratios were explored as a diagnostic parameter using receiver operation curve (ROC) analysis. A new bioinformatics method (MiRImpact) was applied to evaluate the biological significance of the observed expression alterations. Coupled experimental and computational approaches identified reciprocal dysregulation of miR-146b and miR-451 as important attributes of follicular cell malignant transformation and follicular thyroid cancer progression. Thus, evaluation of combined dysregulation of miRNAs relevant to invasion and metastasis can help to distinguish truly malignant follicular thyroid cancer from indolent follicular adenoma. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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15 pages, 4494 KiB  
Article
The Role of Methionine Aminopeptidase 2 in Lymphangiogenesis
by Rawnaq Esa, Eliana Steinberg, Dvir Dror, Ouri Schwob, Mehrdad Khajavi, Miriam Maoz, Yael Kinarty, Adi Inbal, Aviad Zick and Ofra Benny
Int. J. Mol. Sci. 2020, 21(14), 5148; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21145148 - 21 Jul 2020
Cited by 13 | Viewed by 3063
Abstract
During the metastasis process, tumor cells invade the blood circulatory system directly from venous capillaries or indirectly via lymphatic vessels. Understanding the relative contribution of each pathway and identifying the molecular targets that affect both processes is critical for reducing cancer spread. Methionine [...] Read more.
During the metastasis process, tumor cells invade the blood circulatory system directly from venous capillaries or indirectly via lymphatic vessels. Understanding the relative contribution of each pathway and identifying the molecular targets that affect both processes is critical for reducing cancer spread. Methionine aminopeptidase 2 (MetAp2) is an intracellular enzyme known to modulate angiogenesis. In this study, we investigated the additional role of MetAp2 in lymphangiogenesis. A histological staining of tumors from human breast-cancer donors was performed in order to detect the level and the localization of MetAp2 and lymphatic capillaries. The basal enzymatic level and activity in vascular and lymphatic endothelial cells were compared, followed by loss of function studies determining the role of MetAp2 in lymphangiogenesis in vitro and in vivo. The results from the histological analyses of the tumor tissues revealed a high MetAp2 expression, with detectable sites of co-localization with lymphatic capillaries. We showed slightly reduced levels of the MetAp2 enzyme and MetAp2 mRNA expression and activity in primary lymphatic cells when compared to the vascular endothelial cells. The genetic and biochemical manipulation of MetAp2 confirmed the dual activity of the enzyme in both vascular and lymphatic remodulation in cell function assays and in a zebrafish model. We found that cancer-related lymphangiogenesis is inhibited in murine models following MetAp2 inhibition treatment. Taken together, our study provides an indication that MetAp2 is a significant contributor to lymphangiogenesis and carries a dual role in both vascular and lymphatic capillary formation. Our data suggests that MetAp2 inhibitors can be effectively used as anti-metastatic broad-spectrum drugs. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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17 pages, 8872 KiB  
Article
Suppression of PKCδ/NF-κB Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated with Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo
by Chun-Min Su, Yueh-Shan Weng, Lin-Yen Kuan, Jiann-Hwa Chen and Fei-Ting Hsu
Int. J. Mol. Sci. 2020, 21(10), 3527; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21103527 - 16 May 2020
Cited by 31 | Viewed by 3523
Abstract
Magnolol is one of the hydroxylated biphenyl compounds from the root and stem bark of Magnolia officinalis, which shown to possess anti-colorectal cancer (CRC) effects. However, the regulatory mechanism of magnolol on apoptosis and NF-κB signaling in human CRC has not been [...] Read more.
Magnolol is one of the hydroxylated biphenyl compounds from the root and stem bark of Magnolia officinalis, which shown to possess anti-colorectal cancer (CRC) effects. However, the regulatory mechanism of magnolol on apoptosis and NF-κB signaling in human CRC has not been elucidated. Thus, we investigated the inhibitory mechanism of magnolol on human and mouse CRC (HT-29 and CT-26) in vitro and in vivo. Results from reporter gene assay indicated that both magnolol and rottlerin (PKCδ inhibitor) reduced the endogenous NF-κB activity. In addition, indolactam V (PKCδ activator)-induced NF-κB signaling was significantly suppressed with both magnolol and rottlerin treatment. Results from Western blotting also indicated that phosphorylation of PKCδ and NF-κB -related proteins involved in tumor progression were effectively decreased by magnolol treatment. The invasion capacity of CRC cells was also attenuated by both magnolol and rottlerin. Furthermore, magnolol triggered Fas/Fas-L mediated extrinsic apoptosis and mitochondria mediated intrinsic apoptosis were validated by flow cytometry. Most importantly, tumor growth in both HT-29 and CT-26 bearing mice were suppressed by magnolol, but no pathologic change was detected in mice kidney, spleen, and liver. As confirmed by immunohistochemistry (IHC) staining from tumor tissue, PKCδ/NF-κB signaling and downstream proteins expression were decreased, while apoptotic proteins expression was increased in the magnolol treated group. According to these results, we suggest that the induction of apoptosis through extrinsic/intrinsic pathways and the blockage of PKCδ/NF-κB signaling are associated with the magnolol-inhibited progression of CRC. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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Review

Jump to: Editorial, Research

32 pages, 5669 KiB  
Review
RAGE Signaling in Melanoma Tumors
by Olamide T. Olaoba, Sultan Kadasah, Stefan W. Vetter and Estelle Leclerc
Int. J. Mol. Sci. 2020, 21(23), 8989; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21238989 - 26 Nov 2020
Cited by 13 | Viewed by 3423
Abstract
Despite recent progresses in its treatment, malignant cutaneous melanoma remains a cancer with very poor prognosis. Emerging evidences suggest that the receptor for advance glycation end products (RAGE) plays a key role in melanoma progression through its activation in both cancer and stromal [...] Read more.
Despite recent progresses in its treatment, malignant cutaneous melanoma remains a cancer with very poor prognosis. Emerging evidences suggest that the receptor for advance glycation end products (RAGE) plays a key role in melanoma progression through its activation in both cancer and stromal cells. In tumors, RAGE activation is fueled by numerous ligands, S100B and HMGB1 being the most notable, but the role of many other ligands is not well understood and should not be underappreciated. Here, we provide a review of the current role of RAGE in melanoma and conclude that targeting RAGE in melanoma could be an approach to improve the outcomes of melanoma patients. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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44 pages, 2054 KiB  
Review
LncRNAs in Ovarian Cancer Progression, Metastasis, and Main Pathways: ceRNA and Alternative Mechanisms
by Eleonora A. Braga, Marina V. Fridman, Alexey A. Moscovtsev, Elena A. Filippova, Alexey A. Dmitriev and Nikolay E. Kushlinskii
Int. J. Mol. Sci. 2020, 21(22), 8855; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228855 - 23 Nov 2020
Cited by 126 | Viewed by 6602
Abstract
Ovarian cancer (OvCa) develops asymptomatically until it reaches the advanced stages with metastasis, chemoresistance, and poor prognosis. Our review focuses on the analysis of regulatory long non-coding RNAs (lncRNAs) competing with protein-coding mRNAs for binding to miRNAs according to the model of competitive [...] Read more.
Ovarian cancer (OvCa) develops asymptomatically until it reaches the advanced stages with metastasis, chemoresistance, and poor prognosis. Our review focuses on the analysis of regulatory long non-coding RNAs (lncRNAs) competing with protein-coding mRNAs for binding to miRNAs according to the model of competitive endogenous RNA (ceRNA) in OvCa. Analysis of publications showed that most lncRNAs acting as ceRNAs participate in OvCa progression: migration, invasion, epithelial-mesenchymal transition (EMT), and metastasis. More than 30 lncRNAs turned out to be predictors of survival and/or response to therapy in patients with OvCa. For a number of oncogenic (CCAT1, HOTAIR, NEAT1, and TUG1 among others) and some suppressive lncRNAs, several lncRNA/miRNA/mRNA axes were identified, which revealed various functions for each of them. Our review also considers examples of alternative mechanisms of actions for lncRNAs besides being ceRNAs, including binding directly to mRNA or protein, and some of them (DANCR, GAS5, MALAT1, and UCA1 among others) act by both mechanisms depending on the target protein. A systematic analysis based on the data from literature and Panther or KEGG (Kyoto Encyclopedia of Genes and Genomes) databases showed that a significant part of lncRNAs affects the key pathways involved in OvCa metastasis, EMT, and chemoresistance. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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20 pages, 1072 KiB  
Review
How to Predict Metastasis in Luminal Breast Cancer? Current Solutions and Future Prospects
by Sylwia Tabor, Małgorzata Szostakowska-Rodzos, Anna Fabisiewicz and Ewa A. Grzybowska
Int. J. Mol. Sci. 2020, 21(21), 8415; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218415 - 09 Nov 2020
Cited by 15 | Viewed by 4124
Abstract
Breast cancer metastasis is the main cause of breast cancer mortality. Luminal breast cancer represents the majority of breast cancer cases and, despite relatively good prognosis, its heterogeneity creates problems with a proper stratification of patients and correct identification of the group with [...] Read more.
Breast cancer metastasis is the main cause of breast cancer mortality. Luminal breast cancer represents the majority of breast cancer cases and, despite relatively good prognosis, its heterogeneity creates problems with a proper stratification of patients and correct identification of the group with a high risk of metastatic relapse. Current prognostic tools are based on the analysis of the primary tumor and, despite their undisputed power of prediction, they might be insufficient to foresee the relapse in an accurate and precise manner, especially if the relapse occurs after a long period of dormancy, which is very common in luminal breast cancer. New approaches tend to rely on body fluid analyses, which have the advantage of being non-invasive and versatile and may be repeated and used for monitoring the disease in the long run. In this review we describe the current, newly-developed, and only-just-discovered methods which are or may become useful in the assessment of the probability of the relapse. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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22 pages, 2415 KiB  
Review
Neurobiology of Cancer: The Role of β-Adrenergic Receptor Signaling in Various Tumor Environments
by Boris Mravec, Lubica Horvathova and Luba Hunakova
Int. J. Mol. Sci. 2020, 21(21), 7958; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217958 - 26 Oct 2020
Cited by 48 | Viewed by 4137
Abstract
The development and progression of cancer depends on both tumor micro- and macroenvironments. In addition, psychosocial and spiritual “environments” might also affect cancer. It has been found that the nervous system, via neural and humoral pathways, significantly modulates processes related to cancer at [...] Read more.
The development and progression of cancer depends on both tumor micro- and macroenvironments. In addition, psychosocial and spiritual “environments” might also affect cancer. It has been found that the nervous system, via neural and humoral pathways, significantly modulates processes related to cancer at the level of the tumor micro- and macroenvironments. The nervous system also mediates the effects of psychosocial and noetic factors on cancer. Importantly, data accumulated in the last two decades have clearly shown that effects of the nervous system on cancer initiation, progression, and the development of metastases are mediated by the sympathoadrenal system mainly via β-adrenergic receptor signaling. Here, we provide a new complex view of the role of β-adrenergic receptor signaling within the tumor micro- and macroenvironments as well as in mediating the effects of the psychosocial and spiritual environments. In addition, we describe potential preventive and therapeutic implications. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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29 pages, 2158 KiB  
Review
New Insights into Therapy-Induced Progression of Cancer
by Polina V. Shnaider, Olga M. Ivanova, Irina K. Malyants, Ksenia S. Anufrieva, Ilya A. Semenov, Marat S. Pavlyukov, Maria A. Lagarkova, Vadim M. Govorun and Victoria O. Shender
Int. J. Mol. Sci. 2020, 21(21), 7872; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217872 - 23 Oct 2020
Cited by 13 | Viewed by 3544
Abstract
The malignant tumor is a complex heterogeneous set of cells functioning in a no less heterogeneous microenvironment. Like any dynamic system, cancerous tumors evolve and undergo changes in response to external influences, including therapy. Initially, most tumors are susceptible to treatment. However, remaining [...] Read more.
The malignant tumor is a complex heterogeneous set of cells functioning in a no less heterogeneous microenvironment. Like any dynamic system, cancerous tumors evolve and undergo changes in response to external influences, including therapy. Initially, most tumors are susceptible to treatment. However, remaining cancer cells may rapidly reestablish the tumor after a temporary remission. These new populations of malignant cells usually have increased resistance not only to the first-line agent, but also to the second- and third-line drugs, leading to a significant decrease in patient survival. Multiple studies describe the mechanism of acquired therapy resistance. In past decades, it became clear that, in addition to the simple selection of pre-existing resistant clones, therapy induces a highly complicated and tightly regulated molecular response that allows tumors to adapt to current and even subsequent therapeutic interventions. This review summarizes mechanisms of acquired resistance, such as secondary genetic alterations, impaired function of drug transporters, and autophagy. Moreover, we describe less obvious molecular aspects of therapy resistance in cancers, including epithelial-to-mesenchymal transition, cell cycle alterations, and the role of intercellular communication. Understanding these molecular mechanisms will be beneficial in finding novel therapeutic approaches for cancer therapy. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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17 pages, 1685 KiB  
Review
Targeting Hypoxia-Driven Metabolic Reprogramming to Constrain Tumor Progression and Metastasis
by Marisol Miranda-Galvis and Yong Teng
Int. J. Mol. Sci. 2020, 21(15), 5487; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21155487 - 31 Jul 2020
Cited by 31 | Viewed by 4176
Abstract
Hypoxia in locally advanced solid tumors develops due to uncontrollable cell proliferation, altered metabolism, and the severe structural and functional abnormality of the tumor vasculature, leading to an imbalance between oxygen supply and consumption in the fast-growing tumors and negative impact on the [...] Read more.
Hypoxia in locally advanced solid tumors develops due to uncontrollable cell proliferation, altered metabolism, and the severe structural and functional abnormality of the tumor vasculature, leading to an imbalance between oxygen supply and consumption in the fast-growing tumors and negative impact on the therapeutic outcome. Several hypoxia-responsive molecular determinants, such as hypoxia-inducible factors, guide the cellular adaptation to hypoxia by gene activation, which is critical for promoting malignant progression in the hostile tumor microenvironment. Over time, a large body of evidence exists to suggest that tumor hypoxia also influences the tumor metabolic reprogramming, resulting in neoangiogenesis, metastasis, and immune evasion. In this respect, our review aims to understand the biological processes, key events, and consequences regarding the hypoxia-driven metabolic adaptation of tumor cells. We also assess the potential therapeutic impact of hypoxia and highlight our review by discussing possible therapeutic strategies targeting hypoxia, which would advance the current understanding of hypoxia-associated tumor propagation and malignant progression and improve the management of tumor hypoxia. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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17 pages, 2893 KiB  
Review
Epigenetic Landscape in Pancreatic Ductal Adenocarcinoma: On the Way to Overcoming Drug Resistance?
by Sona Ciernikova, Julie Earl, María Laura García Bermejo, Viola Stevurkova, Alfredo Carrato and Bozena Smolkova
Int. J. Mol. Sci. 2020, 21(11), 4091; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114091 - 08 Jun 2020
Cited by 17 | Viewed by 5482
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive solid malignancies due to the rapid rate of metastasis and high resistance to currently applied cancer therapies. The complex mechanism underlying the development and progression of PDAC includes interactions between genomic, epigenomic, and [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive solid malignancies due to the rapid rate of metastasis and high resistance to currently applied cancer therapies. The complex mechanism underlying the development and progression of PDAC includes interactions between genomic, epigenomic, and signaling pathway alterations. In this review, we summarize the current research findings on the deregulation of epigenetic mechanisms in PDAC and the influence of the epigenome on the dynamics of the gene expression changes underlying epithelial–mesenchymal transition (EMT), which is responsible for the invasive phenotype of cancer cells and, therefore, their metastatic potential. More importantly, we provide an overview of the studies that uncover potentially actionable pathways. These studies provide a scientific basis to test epigenetic drug efficacy in synergy with other anticancer therapies in future clinical trials, in order to reverse acquired therapy resistance. Thus, epigenomics has the potential to generate relevant new knowledge of both a biological and clinical impact. Moreover, the potential, hurdles, and challenges of predictive biomarker discoveries will be discussed, with a special focus on the promise of liquid biopsies. Full article
(This article belongs to the Special Issue Attacking Cancer Progression and Metastasis)
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