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 459

Special Issue Editors


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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
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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

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Keywords

  • cancer
  • signalling
  • metastasis
  • tumorigenesis
  • cancer targeting

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Published Papers (1 paper)

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Research

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 365
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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