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Biology
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Signalling Pathways in Cancer and Disease
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Signalling Pathways in Cancer and Disease

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 11719

Special Issue Editors

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; drug repurposing in cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Nadine Wehida

E-Mail Website
Guest Editor Assistant
Department of Biomolecular Sciences, School of Life Sciences, Pharmacy and Chemistry, Kingston University London, Kingston-upon-Thames KT1 2EE, UK
Interests: breast; cancer; non-coding; RNA; diagnostic; H19; microRNA-675; microRNA let 7; CA 15-3; drug repurposing in cancer

Special Issue Information

Dear Colleagues,

Cellular signalling pathways are integral to the regulation of essential biological processes across all forms of life and diseases. These pathways govern a wide array of cellular functions, including proliferation, cell–cell adhesion, extracellular matrix interactions, mechanotransduction, polarity establishment, and programmed cell death (apoptosis). The precise orchestration of these processes is critical for maintaining cellular and tissue homeostasis.

Disruptions or aberrations in these key signalling networks can lead to pathological outcomes, most notably cancer. Dysregulated signalling can drive oncogenesis, tumour progression, metastasis, and resistance to therapy. Understanding the molecular underpinnings of these pathways is therefore vital for identifying novel therapeutic targets and developing effective treatment strategies.

This Special Issue invites original article submissions and special reviews that explore the complexity of cellular signalling in the context of cancer. We particularly welcome studies that provide new insights into the mechanisms by which signalling pathways are altered in malignancy, as well as those that highlight innovative approaches to modulating these pathways for therapeutic benefit, to ensure that we can look at treating this debilitating disease with different methods.

Our goal is to advance the current understanding of signalling dynamics in cancer biology and to foster the development of translational strategies aimed at combating this multifaceted disease.

We look forward to your contributions to this Special Issue.

Dr. Ahmed Elbediwy
Guest Editor

Dr. Nadine Wehida
Guest Editor Assistant

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 250 words) can be sent to the Editorial Office for assessment.

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 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
  • signalling
  • metastasis
  • tumorigenesis
  • cancer targeting

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Published Papers (6 papers)

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Research

Jump to: Review

12 pages, 780 KB  
Article
Disease-Relevant Preoperative Serum miRNA Levels in Papillary Thyroid Cancer
by Olga Bourogianni, Eliza Tsitoura, Konstantinos Sifakis, Nikolaos Kapsoritakis, Alexander Karatzanis, Maria Doulaptsi, Katerina Antoniou, Sophia Koukouraki and Emmanuel Prokopakis
Biology 2026, 15(8), 626; https://doi.org/10.3390/biology15080626 - 16 Apr 2026
Viewed by 376
Abstract
Background: Papillary thyroid cancer (PTC) is the most common form of thyroid malignancy, with an incidence that has been steadily rising globally. Early and accurate diagnosis remains crucial for effective treatment and improved outcomes. MicroRNAs (miRNAs), small non-coding RNA molecules that regulate gene [...] Read more.
Background: Papillary thyroid cancer (PTC) is the most common form of thyroid malignancy, with an incidence that has been steadily rising globally. Early and accurate diagnosis remains crucial for effective treatment and improved outcomes. MicroRNAs (miRNAs), small non-coding RNA molecules that regulate gene expression, have emerged as promising biomarkers in cancer research due to their stability and accessibility in serum. In this pilot study we compared the expression of 84 consistently reported, malignancy-associated serum miRNAs in patients with PTC (PTC group) and benign thyroid disease (Control group) as potential PTC markers. Methods: A focused panel containing primer assays for 84 human miRNAs that are consistently reported in the literature as being detectable and differentially expressed in serum in various organ-specific cancers was used to measure miRNA levels in serum samples from PTC (n = 8) and benign thyroid disease (n = 6) patients prior to thyroidectomy. Results: Among the 84 miRNAs analyzed, a panel of ten miRNAs showed numerical trends of differential expression between the two groups, including three upregulated (hsa-miR-150-5p, hsa-miR-21-5p, hsa-miR-23a-3p) and seven downregulated miRNAs (hsa-miR-17-5p, hsa-miR-17-3p, hsa-miR-200c-3p, hsa-miR-296-5p, hsa-miR-574-3p, hsa-miR-885-5p, hsa-miR-130-3p). The serum expression levels of hsa-miR-23a-3p were markedly elevated in patients with malignant nodules compared with those with benign lesions, while hsa-miR-574-3p was significantly downregulated in the PTC group. Conclusions: These findings warrant further investigation of hsa-miR-23a-3p and hsa-miR-574-3p in larger cohorts of patients with PTC to validate their potential clinical relevance. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
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18 pages, 1463 KB  
Article
Hypoxia-Driven Extracellular Vesicles Promote Pro-Metastatic Signalling in LNCaP Cells via Wnt and EMT Pathways
by Melissa Santos, Khansa Bukhari, Irem Peker-Eyüboğlu, Igor Kraev, Dafydd Alwyn Dart, Sigrun Lange and Pinar Uysal-Onganer
Biology 2025, 14(9), 1135; https://doi.org/10.3390/biology14091135 - 27 Aug 2025
Viewed by 1814
Abstract
Prostate cancer (PCa) progression is shaped by the tumour microenvironment, where hypoxia promotes aggressiveness and contributes to therapy resistance. Extracellular vesicles (EVs), secreted under hypoxia, can deliver modified bioactive cargo that reprograms recipient cells. This study examined whether EVs from hypoxia-conditioned metastatic PCa [...] Read more.
Prostate cancer (PCa) progression is shaped by the tumour microenvironment, where hypoxia promotes aggressiveness and contributes to therapy resistance. Extracellular vesicles (EVs), secreted under hypoxia, can deliver modified bioactive cargo that reprograms recipient cells. This study examined whether EVs from hypoxia-conditioned metastatic PCa cells enhance malignant traits in cancerous and non-tumorigenic prostate cell lines via Wnt signalling and epithelial–mesenchymal transition (EMT). EVs from PC3 cells cultured under hypoxia (1% O2) or normoxia (21% O2) as control were applied to LNCaP (low metastatic potential) and PNT2 (non-tumorigenic) cells. PC3 hypoxia-derived EVs increased HIF-1α, upregulated mesenchymal markers (Vimentin, N-cadherin) and Wnt-related genes (Wnt3A, Wnt5A, Fzd7), and suppressed the epithelial marker E-cadherin. Functional assessment showed that LNCaP cells treated with PC3 hypoxia EVs showed greater motility and invasiveness, and PNT2 cells displayed transcriptomic reprogramming. These findings show that hypoxia-driven EVs can propagate pro-metastatic signalling in less aggressive and normal prostate cells. The findings highlight EVs as a potential therapeutic target in PCa progression. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
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Review

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30 pages, 446 KB  
Review
The Roles of Sirt1 in Breast and Gynecologic Malignancies
by Jianmin Ding, Matthew T. Ye and Songlin Zhang
Biology 2025, 14(11), 1510; https://doi.org/10.3390/biology14111510 - 28 Oct 2025
Cited by 4 | Viewed by 1815
Abstract
Sirtuin 1 (SIRT1), an NAD+-dependent histone deacetylase, exerts complex and context-dependent effects in breast and gynecological cancers. By deacetylating histone and non-histone proteins such as p53, FOXO, and NF-κB, SIRT1 regulates essential processes including DNA repair, apoptosis, metabolism, and stress response. [...] Read more.
Sirtuin 1 (SIRT1), an NAD+-dependent histone deacetylase, exerts complex and context-dependent effects in breast and gynecological cancers. By deacetylating histone and non-histone proteins such as p53, FOXO, and NF-κB, SIRT1 regulates essential processes including DNA repair, apoptosis, metabolism, and stress response. In breast cancer, SIRT1 may act as a tumor suppressor in early stages by maintaining genomic stability but promotes epithelial–mesenchymal transition, metastasis, and chemoresistance in aggressive subtypes such as triple-negative breast cancer. Similarly, in gynecological cancers, SIRT1 displays dual roles: promoting proliferation via estrogen signaling and p53/FOXO1 inhibition in Type I endometrial cancer yet potentially supporting DNA repair in high-grade Type II tumors. Its overexpression in ovarian and cervical cancers is linked to enhanced survival and drug resistance. Preclinical studies show that pharmacological inhibition of SIRT1 (e.g., with EX-527 or cambinol) restores chemosensitivity and reduces tumor cell viability, suggesting potential for SIRT1 inhibitors as adjuncts in cancer therapy. However, clinical trials specifically targeting SIRT1 in these cancers remain limited. Further investigation is needed to define therapeutic windows, molecular contexts, and combination strategies that could optimize SIRT1-targeted therapies. This review summarizes the current understanding of SIRT1’s roles in breast and gynecologic malignancies. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
24 pages, 2368 KB  
Review
Targeting C3a and C5a Signaling—A Game Changer for Cancer Therapy?
by Hunter Hudgins, Valeria Molina, Stanley Wiernicki, Kenneth Okwuegbe, Xiaodong Feng and Hongbin Wang
Biology 2025, 14(11), 1491; https://doi.org/10.3390/biology14111491 - 25 Oct 2025
Cited by 2 | Viewed by 2611
Abstract
Emerging evidence reveals a significant shift in understanding the complement system’s role in cancer, where activation of a complement within the tumor microenvironment (TME) fuels tumor growth and metastasis instead of suppressing it. Research highlights C3a and C5a anaphylatoxins as key drivers of [...] Read more.
Emerging evidence reveals a significant shift in understanding the complement system’s role in cancer, where activation of a complement within the tumor microenvironment (TME) fuels tumor growth and metastasis instead of suppressing it. Research highlights C3a and C5a anaphylatoxins as key drivers of cancer progression, showing that the blockade of their signaling pathways can inhibit tumor growth and metastasis. By interacting with immune cells in the TME, including tumor-associated macrophages (TAMs), T cells, and myeloid-derived suppressor cells, C3a and C5a promote immunosuppression, thereby driving cancer cell proliferation, angiogenesis, and metastasis. However, conflicting findings persist, despite growing evidence supporting the role of C3a and C5a in tumor progression and the potential therapeutic benefits of targeting pathological complement activation. This paper presents a systematic review of studies examining the activation of the complement system and the role of the C3a and C5a signaling pathways in the TME, focusing on their effects on tumor progression, their interactions with TME components, and the potential for targeting these signaling pathways to boost anti-tumor immune responses. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
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26 pages, 2624 KB  
Review
The Dual Role of RASSF4 in Tumorigenesis: Mechanisms and Epigenetic Targeting Strategies
by Rui Tian, Yixin Wu, Wenbin Yuan, Lingli Tian, Rui Zhang, Hao Lyu, Shuai Xiao, Dong Guo, Qi Zhang, Declan William Ali, Marek Michalak, Cefan Zhou, Jingfeng Tang and Xing-Zhen Chen
Biology 2025, 14(9), 1289; https://doi.org/10.3390/biology14091289 - 18 Sep 2025
Viewed by 1621
Abstract
RASSF4 is a key member of the Ras-associated domain family (RASSF) that exhibits dual functionality in tumorigenesis, playing critical yet context-dependent roles in various malignancies. Its expression is epigenetically regulated through promoter hypermethylation, histone modifications, and microRNAs including miR-155 and miR-196a-5p, which directly [...] Read more.
RASSF4 is a key member of the Ras-associated domain family (RASSF) that exhibits dual functionality in tumorigenesis, playing critical yet context-dependent roles in various malignancies. Its expression is epigenetically regulated through promoter hypermethylation, histone modifications, and microRNAs including miR-155 and miR-196a-5p, which directly target its 3′ untranslated region. In most cancers, such as non-small cell lung cancer (NSCLC) and gastric adenocarcinoma (GAC), RASSF4 acts as a tumor suppressor by inhibiting the RAS/MAPK pathway while activating the Hippo signaling cascade, ultimately inducing cell cycle arrest and apoptosis. Conversely, in aRMS, RASSF4 is upregulated by the PAX3-FOXO1 fusion oncoprotein and promotes tumor growth through MST1 inhibition and subsequent YAP activation. This review systematically analyzes current evidence regarding RASSF4’s complex regulatory mechanisms and clinical significance. We propose targeted therapeutic strategies including epigenetic reactivation, gene intervention, and combination therapies. Furthermore, we identify RASSF4 as a promising diagnostic biomarker and therapeutic target based on integrated mechanistic and clinical evidence. Future research should focus on elucidating context-dependent regulatory switches, developing targeted delivery systems, and validating clinical utility through prospective trials. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
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17 pages, 551 KB  
Review
Stabilin-1 in Tumor-Associated Macrophages: A Potential Therapeutic Target in Cancer Immunotherapy
by Jampa Lhamo Gurung, Raju Lama Tamang, Lepakshe Madduri, Robert G. Bennett, Edward N. Harris, Paul W. Denton and Benita McVicker
Biology 2025, 14(9), 1198; https://doi.org/10.3390/biology14091198 - 5 Sep 2025
Cited by 3 | Viewed by 2980
Abstract
Stabilin-1 (STAB1) is a multifunctional scavenger receptor expressed by endothelial cells of the liver, spleen, lymph nodes, bone marrow and a subset of macrophages. STAB1 interacts with different ligands and modulates a wide range of functions including cell trafficking, endocytosis, homeostasis, angiogenesis, and [...] Read more.
Stabilin-1 (STAB1) is a multifunctional scavenger receptor expressed by endothelial cells of the liver, spleen, lymph nodes, bone marrow and a subset of macrophages. STAB1 interacts with different ligands and modulates a wide range of functions including cell trafficking, endocytosis, homeostasis, angiogenesis, and tumor vascularization. The role of STAB1 in cancer progression and metastasis first became evident in Stab1 knockout (KO) mice, which developed smaller primary tumors and metastatic foci for some cancers. To date, various clinical cohorts and preclinical rodent studies have shown that STAB1 inhibition is associated with elevated anti-tumor T-cell responses. Moreover, human trials using anti-STAB1 antibody treatment indicate a shift towards immune activation and the potential to overcome cancer treatment resistance experienced with other immunotherapies. Although the role of STAB1 in cancer development and metastasis remains to be defined, STAB1 signaling in tumor-associated macrophages and downstream immune modulation are thought to be crucial mechanisms. Herein, we discuss the role of STAB1 in tumor-associated macrophages in relationship to disease progression and patient outcome. Full article
(This article belongs to the Special Issue Signalling Pathways in Cancer and Disease)
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