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Cells
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Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways...
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Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell and Gene Therapy".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 4352

Special Issue Editors

Dr. Daria A. Chudakova

E-Mail Website
Guest Editor
Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia
Interests: cancer biology; ageing; cell fate, reprogramming and regeneration; epigenetics
Dr. Kazuyuki Kitatani

E-Mail Website
Guest Editor
Laboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata 573‐0101, Japan
Interests: sphingolipids; ceramides; sphingotherapy; cancer therapy; cancer biology; cancer metastasis; cellular signaling; cell death; necroptosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The study of human neoplastic diseases is a burgeoning and blazing-hot area of biomedicine. However, despite significant advances in this field, some patients are misdiagnosed and, for some, no effective treatments currently available. This Special Issue will provide an overview on the emerging therapeutic targets, approaches and molecular tools as well as novel genetic markers and signaling pathways in neoplasms (benign, malignant and of uncertain or unknown behavior). We welcome pioneering research-based works looking at the subject from a new angle. We also encourage the authors to present their review articles and formulate principally novel views on a subject, as long as their hypothesis and opinions are strongly supported by the body of the previously published experimental data. Research with direct clinical and translational application opening novel curative and diagnostic options is of particular interest.

Dr. Daria A. Chudakova
Dr. Kazuyuki Kitatani
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • neoplasms
  • personalized medicine
  • genetic markers
  • next-generation sequencing (NGS)
  • whole-genome sequencing
  • signaling pathways in cancer
  • novel therapeutic targets
  • drug development

Published Papers (4 papers)

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Research

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19 pages, 9808 KiB  
Article
Decorin (DCN) Downregulation Activates Breast Stromal Fibroblasts and Promotes Their Pro-Carcinogenic Effects through the IL-6/STAT3/AUF1 Signaling
by Wafaa A. Aljagthmi, Manal A. Alasmari, Maha H. Daghestani, Layla A. Al-Kharashi, Falah H. Al-Mohanna and Abdelilah Aboussekhra
Cells 2024, 13(8), 680; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13080680 - 14 Apr 2024
Viewed by 896
Abstract
Decorin (DCN), a member of the small leucine-rich proteoglycan gene family, is secreted from stromal fibroblasts with non-cell-autonomous anti-breast-cancer effects. Therefore, in the present study, we sought to elucidate the function of decorin in breast stromal fibroblasts (BSFs). We first showed DCN downregulation [...] Read more.
Decorin (DCN), a member of the small leucine-rich proteoglycan gene family, is secreted from stromal fibroblasts with non-cell-autonomous anti-breast-cancer effects. Therefore, in the present study, we sought to elucidate the function of decorin in breast stromal fibroblasts (BSFs). We first showed DCN downregulation in active cancer-associated fibroblasts (CAFs) compared to their adjacent tumor counterpart fibroblasts at both the mRNA and protein levels. Interestingly, breast cancer cells and the recombinant IL-6 protein, both known to activate fibroblasts in vitro, downregulated DCN in BSFs. Moreover, specific DCN knockdown in breast fibroblasts modulated the expression/secretion of several CAF biomarkers and cancer-promoting proteins (α-SMA, FAP- α, SDF-1 and IL-6) and enhanced the invasion/proliferation abilities of these cells through activation of the STAT3/AUF1 signaling. Furthermore, DCN-deficient fibroblasts promoted the epithelial-to-mesenchymal transition and stemness processes in BC cells in a paracrine manner, which increased their resistance to cisplatin. These DCN-deficient fibroblasts also enhanced angiogenesis and orthotopic tumor growth in mice in a paracrine manner. On the other hand, ectopic expression of DCN in CAFs suppressed their active features and their paracrine pro-carcinogenic effects. Together, the present findings indicate that endogenous DCN suppresses the pro-carcinogenic and pro-metastatic effects of breast stromal fibroblasts. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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18 pages, 19121 KiB  
Article
Analysis of the Expression of LSF Transcription Factor in the Regulation of Transcription and TSG101 during the Neoplastic Transformation of Endometrial Cells
by Rafał Ziemiński, Aleksandra Stupak, Maciej Kwiatek, Tomasz Gęca, Alicja Warowicka, Karolina Hejne, Anna Kwaśniewska, Anna Goździcka-Józefiak and Wojciech Kwaśniewski
Cells 2024, 13(7), 580; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13070580 - 26 Mar 2024
Viewed by 471
Abstract
Previous research indicates that carcinogenesis involves disrupting the functions of numerous genes, including factors involved in the regulation of transcription and cell proliferation. For these reasons, in endometrial carcinogenesis, we decided to investigate the expression of TSG101 (a suppressor of tumor transformation) and [...] Read more.
Previous research indicates that carcinogenesis involves disrupting the functions of numerous genes, including factors involved in the regulation of transcription and cell proliferation. For these reasons, in endometrial carcinogenesis, we decided to investigate the expression of TSG101 (a suppressor of tumor transformation) and LSF (a transcription factor involved in numerous cellular processes, such as cell cycle regulation, cell growth, development, and apoptosis). LSF may be involved in the regulation of TSG101 expression. The research material consisted of endometrial cancer samples from 60 patients. The control group consisted of normal endometrium samples donated by 60 women undergoing surgery for benign diseases of the female reproductive organs. The samples were subjected to immunohistochemical staining with antibodies specific to TSG101 and LSF. Specific antibodies were used to identify TSG101 and LSF in the examined histopathological preparations. An approximately 14-fold lower risk of endometrial cancer development was observed in patients with TSG expression in more than 75% of the assessed cells (4% vs. 36%; OR = 0.07; p = 0.0182). There was a four-fold lower risk of endometrial cancer development in patients with LSF expression in more than 50% of the assessed cells (32% vs. 64%; OR = 0.26; p = 0.0262). A more than three-fold lower risk of endometrial cancer development was observed in patients with LSF expression in more than 75% of the assessed cells (24% vs. 52%; OR = 0.29; p = 0.0454). Endometrial cancer was diagnosed in those with a lower level of TSG101 expression than in those with a cancer-free endometrium. Decreased expression of TSG101 may be a marker of endometrial cancer, and increased expression of LSF when diagnosed with endometrial cancer may indicate greater advancement of the disease. These markers might be used as diagnostic and prognostic markers—however, there is a lack of a correlation between them. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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12 pages, 3459 KiB  
Article
Pronecroptotic Therapy Using Ceramide Nanoliposomes Is Effective for Triple-Negative Breast Cancer Cells
by Yuki Ohya, Yuri Ogiso, Masaya Matsuda, Harumi Sakae, Kentaro Nishida, Yasuhiro Miki, Todd E. Fox, Mark Kester, Wataru Sakamoto, Takeshi Nabe and Kazuyuki Kitatani
Cells 2024, 13(5), 405; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13050405 - 26 Feb 2024
Viewed by 761
Abstract
Regulated necrosis, termed necroptosis, represents a potential therapeutic target for refractory cancer. Ceramide nanoliposomes (CNLs), considered potential chemotherapeutic agents, induce necroptosis by targeting the activating protein mixed lineage kinase domain-like protein (MLKL). In the present study, we examined the potential of pronecroptotic therapy [...] Read more.
Regulated necrosis, termed necroptosis, represents a potential therapeutic target for refractory cancer. Ceramide nanoliposomes (CNLs), considered potential chemotherapeutic agents, induce necroptosis by targeting the activating protein mixed lineage kinase domain-like protein (MLKL). In the present study, we examined the potential of pronecroptotic therapy using CNLs for refractory triple-negative breast cancer (TNBC), for which there is a lack of definite and effective therapeutic targets among the various immunohistological subtypes of breast cancer. MLKL mRNA expression in tumor tissues was significantly higher in TNBC patients than in those with non-TNBC subtypes. Similarly, among the 50 breast cancer cell lines examined, MLKL expression was higher in TNBC-classified cell lines. TNBC cell lines were more susceptible to the therapeutic effects of CNLs than the non-TNBC subtypes of breast cancer cell lines. In TNBC-classified MDA-MB-231 cells, the knockdown of MLKL suppressed cell death induced by CNLs or the active substance short-chain C6-ceramide. Accordingly, TNBC cells were prone to CNL-evoked necroptotic cell death. These results will contribute to the development of CNL-based pronecroptotic therapy for TNBC. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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Review

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25 pages, 3282 KiB  
Review
Molecular Regulation and Oncogenic Functions of TSPAN8
by Jicheng Yang, Ziyan Zhang, Joanne Shi Woon Lam, Hao Fan and Nai Yang Fu
Cells 2024, 13(2), 193; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13020193 - 19 Jan 2024
Viewed by 1714
Abstract
Tetraspanins, a superfamily of small integral membrane proteins, are characterized by four transmembrane domains and conserved protein motifs that are configured into a unique molecular topology and structure in the plasma membrane. They act as key organizers of the plasma membrane, orchestrating the [...] Read more.
Tetraspanins, a superfamily of small integral membrane proteins, are characterized by four transmembrane domains and conserved protein motifs that are configured into a unique molecular topology and structure in the plasma membrane. They act as key organizers of the plasma membrane, orchestrating the formation of specialized microdomains called “tetraspanin-enriched microdomains (TEMs)” or “tetraspanin nanodomains” that are essential for mediating diverse biological processes. TSPAN8 is one of the earliest identified tetraspanin members. It is known to interact with a wide range of molecular partners in different cellular contexts and regulate diverse molecular and cellular events at the plasma membrane, including cell adhesion, migration, invasion, signal transduction, and exosome biogenesis. The functions of cell-surface TSPAN8 are governed by ER targeting, modifications at the Golgi apparatus and dynamic trafficking. Intriguingly, limited evidence shows that TSPAN8 can translocate to the nucleus to act as a transcriptional regulator. The transcription of TSPAN8 is tightly regulated and restricted to defined cell lineages, where it can serve as a molecular marker of stem/progenitor cells in certain normal tissues as well as tumors. Importantly, the oncogenic roles of TSPAN8 in tumor development and cancer metastasis have gained prominence in recent decades. Here, we comprehensively review the current knowledge on the molecular characteristics and regulatory mechanisms defining TSPAN8 functions, and discuss the potential and significance of TSPAN8 as a biomarker and therapeutic target across various epithelial cancers. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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