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Molecular Signal Transduction in Tumor Progression and Metastasis
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Molecular Signal Transduction in Tumor 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 2022) | Viewed by 10714

Special Issue Editors

Prof. Dr. Karel Smetana, Jr.

E-Mail Website1 Website2 Website3
Guest Editor
1st Faculty Medicine, Institute of Anatomy and BIOCEV, Charles University, Prague 2 and Vestec, Prague, Czech Republic
Interests: tumor microenvironment; cutaneous malignant melanoma; cancer-associated fibroblasts; squamous epithelium; stem cells
Special Issues, Collections and Topics in MDPI journals
Prof. Michal Kolář

E-Mail Website
Guest Editor
Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic
Interests: tumor microenvironment; cancer transcriptomics; genomics; bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Even in this COVID-19 era, cancer represents one of the most relevant medical, social, and economic issues. The epidemic-like occurrence of malignant diseases is associated with many reasons; however, the aging of the population remains one of the main causes. Despite the progress in diagnostics and therapy represented by biological and targeted treatments, new approaches are required that are suitable for elderly and frail patients. One possibility is therapeutic intervention in the signaling network formed between the cancer and non-cancer cells in the tumor microenvironment. This option includes targeting the interactions that maintain stem cell properties of cancer stem cells. Another possibility is the modulation of ligand–receptor interactions and signal transduction in the cells within the cancer ecosystem. Detailed knowledge of this signaling network is necessary, not only to understand the mechanisms of cancer progression and metastasis but also to develop new targeted therapeutic modalities.

Topics of this Special Issue include but are not limited to:

  • Cancer progression and metastasis;
  • Targeted therapy of cancer;
  • Cancer microenvironment;
  • Cancer-associated fibroblasts;
  • Tumor-associated macrophages;
  • Immune cells in cancer ecosystem;
  • Cancer stem cells;
  • Extracellular matrix and cancer;
  • Signal transduction in cancer cells;
  • Receptor modulators.

Prof. Dr. Karel Smetana, Jr.
Prof. Michal Kolář
Guest Editors

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 and metastasis
  • Targeted therapy of cancer
  • Cancer microenvironment
  • Cancer-associated fibroblasts
  • Tumor-associated macrophages
  • Immune cells in cancer ecosystem
  • Cancer stem cells
  • Extracellular matrix and cancer
  • Signal transduction in cancer cell
  • Receptor modulators

Published Papers (3 papers)

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Research

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14 pages, 2274 KiB  
Article
Role of Fibroblast Growth Factors in the Crosstalk of Hepatic Stellate Cells and Uveal Melanoma Cells in the Liver Metastatic Niche
by Tatjana Seitz, Nora John, Judith Sommer, Peter Dietrich, Wolfgang E. Thasler, Arndt Hartmann, Katja Evert, Sven A. Lang, Anja Bosserhoff and Claus Hellerbrand
Int. J. Mol. Sci. 2022, 23(19), 11524; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911524 - 29 Sep 2022
Cited by 4 | Viewed by 1454
Abstract
Hepatic metastasis is the critical factor determining tumor-associated mortality in different types of cancer. This is particularly true for uveal melanoma (UM), which almost exclusively metastasizes to the liver. Hepatic stellate cells (HSCs) are the precursors of tumor-associated fibroblasts and support the growth [...] Read more.
Hepatic metastasis is the critical factor determining tumor-associated mortality in different types of cancer. This is particularly true for uveal melanoma (UM), which almost exclusively metastasizes to the liver. Hepatic stellate cells (HSCs) are the precursors of tumor-associated fibroblasts and support the growth of metastases. However, the underlying mechanisms are widely unknown. Fibroblast growth factor (FGF) signaling is dysregulated in many types of cancer. The aim of this study was to analyze the pro-tumorigenic effects of HSCs on UM cells and the role of FGFs in this crosstalk. Conditioned medium (CM) from activated human HSCs significantly induced proliferation together with enhanced ERK and JNK activation in UM cells. An in silico database analysis revealed that there are almost no mutations of FGF receptors (FGFR) in UM. However, a high FGFR expression was found to be associated with poor survival for UM patients. In vitro, the pro-tumorigenic effects of HSC-CM on UM cells were abrogated by a pharmacological inhibitor (BGJ398) of FGFR1/2/3. The expression analysis revealed that the majority of paracrine FGFs are expressed by HSCs, but not by UM cells, including FGF9. Furthermore, the immunofluorescence analysis indicated HSCs as a cellular source of FGF9 in hepatic metastases of UM patients. Treatment with recombinant FGF9 significantly enhanced the proliferation of UM cells, and this effect was efficiently blocked by the FGFR1/2/3 inhibitor BGJ398. Our study indicates that FGF9 released by HSCs promotes the tumorigenicity of UM cells, and thus suggests FGF9 as a promising therapeutic target in hepatic metastasis. Full article
(This article belongs to the Special Issue Molecular Signal Transduction in Tumor Progression and Metastasis)
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26 pages, 5728 KiB  
Article
Effects of Pubertal Exposure to Butyl Benzyl Phthalate, Perfluorooctanoic Acid, and Zeranol on Mammary Gland Development and Tumorigenesis in Rats
by Yanrong Su, Julia Santucci-Pereira, Nhi M. Dang, Joice Kanefsky, Vishnuprabha Rahulkannan, Meardey Hillegass, Shalina Joshi, Hafsa Gurdogan, Zhen Chen, Vincent Bessonneau, Ruthann Rudel, Jennifer Ser-Dolansky, Sallie S. Schneider and Jose Russo
Int. J. Mol. Sci. 2022, 23(3), 1398; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031398 - 26 Jan 2022
Cited by 6 | Viewed by 3323
Abstract
Endocrine-disrupting chemicals (EDCs)—including butyl benzyl phthalate (BBP), perfluorooctanoic acid (PFOA), and zeranol (α-ZAL, referred to as ZAL hereafter)—can interfere with the endocrine system and produce adverse effects. It remains unclear whether pubertal exposure to low doses of BBP, PFOA, and ZAL has an [...] Read more.
Endocrine-disrupting chemicals (EDCs)—including butyl benzyl phthalate (BBP), perfluorooctanoic acid (PFOA), and zeranol (α-ZAL, referred to as ZAL hereafter)—can interfere with the endocrine system and produce adverse effects. It remains unclear whether pubertal exposure to low doses of BBP, PFOA, and ZAL has an impact on breast development and tumorigenesis. We exposed female Sprague Dawley rats to BBP, PFOA, or ZAL through gavage for 21 days, starting on day 21, and analyzed their endocrine organs, serum hormones, mammary glands, and transcriptomic profiles of the mammary glands at days 50 and 100. We also conducted a tumorigenesis study for rats treated with PFOA and ZAL using a 7,12-dimethylbenz[a]anthracene (DMBA) model. Our results demonstrated that pubertal exposure to BBP, PFOA, and ZAL affected endocrine organs and serum hormones, and induced phenotypic and transcriptomic changes. The exposure to PFOA + ZAL induced the most phenotypic and transcriptomic changes in the mammary gland. PFOA + ZAL downregulated the expression of genes related to development at day 50, whereas it upregulated genes associated with tumorigenesis at day 100. PFOA + ZAL exposure also decreased rat mammary tumor latency, reduced the overall survival of rats after DMBA challenge, and affected the histopathology of mammary tumors. Therefore, our study suggests that exposure to low doses of EDCs during the pubertal period could induce changes in the endocrine system and mammary gland development in rats. The inhibition of mammary gland development by PFOA + ZAL might increase the risk of developing mammary tumors through activation of signaling pathways associated with tumorigenesis. Full article
(This article belongs to the Special Issue Molecular Signal Transduction in Tumor Progression and Metastasis)
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Review

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17 pages, 1418 KiB  
Review
Characteristics of TIMP1, CD63, and β1-Integrin and the Functional Impact of Their Interaction in Cancer
by Beatriz Laís Justo and Miriam Galvonas Jasiulionis
Int. J. Mol. Sci. 2021, 22(17), 9319; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179319 - 27 Aug 2021
Cited by 28 | Viewed by 5322
Abstract
Tissue Inhibitor of Metalloproteases 1, also known as TIMP-1, is named for its well-established function of inhibiting the proteolytic activity of matrix metalloproteases. Given this function, many studies were carried out to verify if TIMP-1 was able to interrupt processes such as tumor [...] Read more.
Tissue Inhibitor of Metalloproteases 1, also known as TIMP-1, is named for its well-established function of inhibiting the proteolytic activity of matrix metalloproteases. Given this function, many studies were carried out to verify if TIMP-1 was able to interrupt processes such as tumor cell invasion and metastasis. In contrast, many studies have shown that TIMP-1 expression is increased in several types of tumors, and this increase was correlated with a poor prognosis and lower survival in cancer patients. Later, it was shown that TIMP-1 is also able to modulate cell behavior through the induction of signaling pathways involved in cell growth, proliferation, and survival. The mechanisms involved in the regulation of the pleiotropic functions of TIMP-1 are still poorly understood. Thus, this review aimed to present literature data that show its ability to form a membrane complex with CD63 and β1-integrin, and point to N-glycosylation as a potential regulatory mechanism of the functions exerted by TIMP-1. This article reviewed the characteristics and functions performed individually by TIMP1, CD63, and β1-integrin, the roles of the TIMP-1/CD63/β1-integrin complex, both in a physiological context and in cancer, and the regulatory mechanisms involved in its assembly. Full article
(This article belongs to the Special Issue Molecular Signal Transduction in Tumor Progression and Metastasis)
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