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Biology
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Cancer and Signalling: Targeting Cellular Pathways
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Cancer and Signalling: Targeting Cellular Pathways

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 4514

Special Issue Editor

Dr. Ahmed Elbediwy

E-Mail Website
Guest Editor
Department of Biomolecular Sciences, Kingston University, Kingston upon Thames KT1 2EE, UK
Interests: Hippo signalling; mechanotransduction; YAP; cancer; polarity; Rho GTPases; signalling; organ growth; extracellular matrix; integrins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Within all types of organisms there are fundamental cellular processes being orchestrated continuously in the background, resulting in the regulation of various signalling pathways. These pathways result in many cellular functions, including proliferation, cell–cell adhesion, extracellular matrix signalling, mechanotransduction, polarity and apoptosis, all of which are fundamental within cells. If these pathways dysfunction, then this can result in disease formation, including cancer. This Special Issue welcomes the submission of articles and reviews which cover a wide range of signalling pathways and examine how any disruption to these pathways can lead to cancer. I hope that we will try to expand upon what is currently known in the signalling field in this Special Issue by looking at new cutting-edge findings, which will hopefully shed some light on how signalling can control cancer progression, and possibly make us understand how we can combat this debilitating disease.

Dr. Ahmed Elbediwy
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. Biology is an international peer-reviewed open access monthly 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

  • Hippo signalling
  • mechanotransduction
  • YAP
  • cancer
  • polarity
  • Rho GTPases
  • signalling, organ growth
  • extracellular matrix
  • integrins

Published Papers (3 papers)

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Research

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22 pages, 3527 KiB  
Article
1,25-Dihydroxyvitamin D3 Suppresses Prognostic Survival Biomarkers Associated with Cell Cycle and Actin Organization in a Non-Malignant African American Prostate Cell Line
by Jabril R. Johnson, Rachel N. Martini, Yate-Ching Yuan, Leanne Woods-Burnham, Mya Walker, Greisha L. Ortiz-Hernandez, Firas Kobeissy, Dorothy Galloway, Amani Gaddy, Chidinma Oguejiofor, Blake Allen, Deyana Lewis, Melissa B. Davis, K. Sean Kimbro, Clayton C. Yates, Adam B. Murphy and Rick A. Kittles
Biology 2024, 13(5), 346; https://doi.org/10.3390/biology13050346 - 15 May 2024
Viewed by 1155
Abstract
Vitamin D3 is a steroid hormone that confers anti-tumorigenic properties in prostate cells. Serum vitamin D3 deficiency has been associated with advanced prostate cancer (PCa), particularly affecting African American (AA) men. Therefore, elucidating the pleiotropic effects of vitamin D on signaling [...] Read more.
Vitamin D3 is a steroid hormone that confers anti-tumorigenic properties in prostate cells. Serum vitamin D3 deficiency has been associated with advanced prostate cancer (PCa), particularly affecting African American (AA) men. Therefore, elucidating the pleiotropic effects of vitamin D on signaling pathways, essential to maintaining non-malignancy, may provide additional drug targets to mitigate disparate outcomes for men with PCa, especially AA men. We conducted RNA sequencing on an AA non-malignant prostate cell line, RC-77N/E, comparing untreated cells to those treated with 10 nM of vitamin D3 metabolite, 1α,25(OH)2D3, at 24 h. Differential gene expression analysis revealed 1601 significant genes affected by 1α,25(OH)2D3 treatment. Pathway enrichment analysis predicted 1α,25(OH)2D3- mediated repression of prostate cancer, cell proliferation, actin cytoskeletal, and actin-related signaling pathways (p < 0.05). Prioritizing genes with vitamin D response elements and associating expression levels with overall survival (OS) in The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA PRAD) cohort, we identified ANLN (Anillin) and ECT2 (Epithelial Cell Transforming 2) as potential prognostic PCa biomarkers. Both genes were strongly correlated and significantly downregulated by 1α,25(OH)2D3 treatment, where low expression was statistically associated with better overall survival outcomes in the TCGA PRAD public cohort. Increased ANLN and ECT2 mRNA gene expression was significantly associated with PCa, and Gleason scores using both the TCGA cohort (p < 0.05) and an AA non-malignant/tumor-matched cohort. Our findings suggest 1α,25(OH)2D3 regulation of these biomarkers may be significant for PCa prevention. In addition, 1α,25(OH)2D3 could be used as an adjuvant treatment targeting actin cytoskeleton signaling and actin cytoskeleton-related signaling pathways, particularly among AA men. Full article
(This article belongs to the Special Issue Cancer and Signalling: Targeting Cellular Pathways)
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Review

Jump to: Research

18 pages, 2795 KiB  
Review
Drug Repurposing: Exploring Potential Anti-Cancer Strategies by Targeting Cancer Signalling Pathways
by Natalia Haddad, Sara Magura Gamaethige, Nadine Wehida and Ahmed Elbediwy
Biology 2024, 13(6), 386; https://doi.org/10.3390/biology13060386 - 28 May 2024
Viewed by 311
Abstract
The repurposing of previously clinically approved drugs as an alternative therapeutic approach to treating disease has gained significant attention in recent years. A multitude of studies have demonstrated various and successful therapeutic interventions with these drugs in a wide range of neoplastic diseases, [...] Read more.
The repurposing of previously clinically approved drugs as an alternative therapeutic approach to treating disease has gained significant attention in recent years. A multitude of studies have demonstrated various and successful therapeutic interventions with these drugs in a wide range of neoplastic diseases, including multiple myeloma, leukaemia, glioblastoma, and colon cancer. Drug repurposing has been widely encouraged due to the known efficacy, safety, and convenience of already established drugs, allowing the bypass of the long and difficult road of lead optimization and drug development. Repurposing drugs in cancer therapy is an exciting prospect due to the ability of these drugs to successfully target cancer-associated genes, often dysregulated in oncogenic signalling pathways, amongst which are the classical cancer signalling pathways; WNT (wingless-related integration type) and Hippo signalling. These pathways play a fundamental role in controlling organ size, tissue homeostasis, cell proliferation, and apoptosis, all hallmarks of cancer initiation and progression. Prolonged dysregulation of these pathways has been found to promote uncontrolled cellular growth and malignant transformation, contributing to carcinogenesis and ultimately leading to malignancy. However, the translation of cancer signalling pathways and potential targeted therapies in cancer treatment faces ongoing challenges due to the pleiotropic nature of cancer cells, contributing to resistance and an increased rate of incomplete remission in patients. This review provides analyses of a range of potential anti-cancer compounds in drug repurposing. It unravels the current understanding of the molecular rationale for repurposing these drugs and their potential for targeting key oncogenic signalling pathways. Full article
(This article belongs to the Special Issue Cancer and Signalling: Targeting Cellular Pathways)
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50 pages, 8349 KiB  
Review
Expanding Roles of the E2F-RB-p53 Pathway in Tumor Suppression
by Yaxuan Zhou, Rinka Nakajima, Mashiro Shirasawa, Mariana Fikriyanti, Lin Zhao, Ritsuko Iwanaga, Andrew P. Bradford, Kenta Kurayoshi, Keigo Araki and Kiyoshi Ohtani
Biology 2023, 12(12), 1511; https://doi.org/10.3390/biology12121511 - 11 Dec 2023
Viewed by 2365
Abstract
The transcription factor E2F links the RB pathway to the p53 pathway upon loss of function of pRB, thereby playing a pivotal role in the suppression of tumorigenesis. E2F fulfills a major role in cell proliferation by controlling a variety of growth-associated genes. [...] Read more.
The transcription factor E2F links the RB pathway to the p53 pathway upon loss of function of pRB, thereby playing a pivotal role in the suppression of tumorigenesis. E2F fulfills a major role in cell proliferation by controlling a variety of growth-associated genes. The activity of E2F is controlled by the tumor suppressor pRB, which binds to E2F and actively suppresses target gene expression, thereby restraining cell proliferation. Signaling pathways originating from growth stimulative and growth suppressive signals converge on pRB (the RB pathway) to regulate E2F activity. In most cancers, the function of pRB is compromised by oncogenic mutations, and E2F activity is enhanced, thereby facilitating cell proliferation to promote tumorigenesis. Upon such events, E2F activates the Arf tumor suppressor gene, leading to activation of the tumor suppressor p53 to protect cells from tumorigenesis. ARF inactivates MDM2, which facilitates degradation of p53 through proteasome by ubiquitination (the p53 pathway). P53 suppresses tumorigenesis by inducing cellular senescence or apoptosis. Hence, in almost all cancers, the p53 pathway is also disabled. Here we will introduce the canonical functions of the RB-E2F-p53 pathway first and then the non-classical functions of each component, which may be relevant to cancer biology. Full article
(This article belongs to the Special Issue Cancer and Signalling: Targeting Cellular Pathways)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Drug Repurposing: Exploring Potential Anti-Cancer Strategies by targeting Cancer Signalling Pathways.
Authors: Natalia Haddad; Sara Magura Gamaethige; Nadine Wehida; Ahmed Elbediwy
Affiliation: Kingston University
Abstract: The repurposing of previously clinically approved drugs as an alternative therapeutic approach to treating disease has gained significant attention in recent years. A multitude of research has demonstrated various and successful therapeutic interventions of these drugs in a wide range of neoplastic diseases, including multiple myeloma, leukemia, glioblastoma, and colon cancer. Drug repurposing has been widely encouraged due to the known efficacy, safety and convenience of already established drugs, allowing the bypass of the long difficult road of lead optimization and drug development. Repurposing drugs in cancer therapy is an exciting prospect due to the ability of these drugs to successfully target cancer-associated genes, often dysregulated in oncogenic signaling pathways, amongst which are the classical cancer signaling pathways WNT (wingless-related integration type) and Hippo signaling. These pathways play a fundamental role in controlling organ size, tissue homeostasis, cell proliferation, and apoptosis, all hallmarks in cancer initiation and progression. Prolonged dysregulation of these pathways has been found to promote uncontrolled cellular growth and malignant transformation, contributing to carcinogenesis ultimately leading to malignancy. However, the translation of cancer signaling pathways and potential targeted therapies in cancer treatment faces ongoing challenges due to the pleiotropic nature of cancer cells, contributing to resistance and an increased rate of incomplete remission in patients. This review provides analyses of a range of potential anti-cancer compounds in drug repurposing. It unravels the current understanding of the molecular rationale for repurposing these drugs and their potential in targeting key oncogenic signaling pathways.

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