Signaling Mechanisms Controlling Cell Fate in Cancer

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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1147

Editors


E-Mail Website
Guest Editor
Division of Biochemistry, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand
Interests: miRNAs; epigenetics; cell signalling; biomarkers; environmental pollutants; natural products

E-Mail Website
Guest Editor
Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
Interests: natural products; molecular biology; cell signaling; biomarkers; miRNAs

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue titled “Signaling Mechanisms Controlling Cell Fate in Cancer”. Cancer progression fundamentally depends on dysregulated signaling pathways that control critical cellular fate decisions between survival, proliferation, differentiation, senescence, and death. Understanding these complex molecular mechanisms is essential for developing effective therapeutic strategies. The intricate interplay between classical signaling networks, epigenetic regulation, microRNA-mediated control, environmental factors, and exposure to environmental pollutants creates a sophisticated regulatory system that determines cancer cell destiny. This research area represents a cornerstone of modern cancer biology, with direct implications for personalized medicine and targeted therapy development.

This Special Issue aims to advance our understanding of how signaling networks and regulatory circuits coordinate in order to determine cancer cell fate, ultimately contributing to the development of more effective, personalized cancer treatments. We seek to compile cutting-edge research that provides mechanistic insights into cell fate control mechanisms and demonstrates clinical relevance or therapeutic potential. The scope aligns perfectly with the Journal of Biology’s focus on molecular and cellular biology, encompassing both fundamental biological processes and their applications in human health.

In this Special Issue, original research articles and reviews are welcome. Research areas may include, but are not limited to, the following:

  • p53, Wnt, Notch, PI3K/AKT, MAPK, and TGF-β signaling pathways in cell fate determination.
  • miRNA-mediated control of signaling pathways and cancer cell fate.
  • Epigenetic regulation of cell fate decisions in cancer.
  • Integrative omics and cell fate in cancer.
  • Tumor microenvironment influences on cancer cell behavior.
  • Environmental pollutants and their impact on cancer cell fate signaling.
  • Natural products and signaling networks governing cell fate in cancer.
  • Metabolic reprogramming affecting cellular destiny.
  • Mechanisms of therapy resistance and cell fate plasticity.
  • Cancer stem cell signaling in initiation and progression.
  • Novel therapeutic targets within cell fate signaling pathways.
  • Biomarkers for predicting treatment response.

We look forward to receiving your contributions.

Dr. Wittaya Chaiwangyen
Dr. Orawan Khantamat
Guest Editors

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Keywords

  • cell fate
  • cancer signaling
  • miRNA
  • p53
  • Wnt
  • apoptosis
  • proliferation
  • differentiation
  • therapy resistance
  • biomarkers

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Published Papers (1 paper)

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Research

34 pages, 3713 KB  
Article
Fucosylation Dynamics as a Critical Determinant of Cancer Cell Fate in Colorectal Carcinoma: Integrating Hallmark Plasticity, Microenvironmental Remodelling, and Therapeutic Resistance
by Abdulaziz Alfahed, Abdulrahman A. Alahmari and Glowi Alasiri
Biology 2026, 15(9), 689; https://doi.org/10.3390/biology15090689 - 28 Apr 2026
Viewed by 703
Abstract
Fucosylation, the enzymatic addition of fucose residues to glycans, modulates receptor signalling and cellular identity in the intestinal epithelium. Its role as an integrative determinant of cancer cell fate in colorectal cancer (CRC) remains undefined. Transcriptomic and clinicopathological data from 976 CRC patients [...] Read more.
Fucosylation, the enzymatic addition of fucose residues to glycans, modulates receptor signalling and cellular identity in the intestinal epithelium. Its role as an integrative determinant of cancer cell fate in colorectal cancer (CRC) remains undefined. Transcriptomic and clinicopathological data from 976 CRC patients across three independent cohorts (TCGA-CRC, CPTAC2-CRC, Sidra-LUMC) were analysed. A curated fucosylation gene set was used to calculate tumour fucosylation scores. Associations with histogenetic status, genomic features, microenvironmental phenotypes, drug resistance programmes, and survival were evaluated using gene set enrichment analysis, multivariable Cox regression, and integrated molecular subtyping. High-fucosylation tumours exhibited elevated epithelial differentiation, MSI-H/BRAF-mutant enrichment, oxidative phosphorylation dominance, the complete absence of EMT and invasion programmes, and favourable prognosis (HR = 0.633, 95% CI: 0.470–0.853, p = 0.003). Low-fucosylation tumours demonstrated mesenchymal phenotypes, TP53 mutations, chromosomal instability, comprehensive multi-family RTK signalling, immune-excluded microenvironments, and poor outcomes. Distinct multidrug resistance programmes emerged: drug efflux in low-fucosylation tumours versus xenobiotic sensing, target bypass, and drug sequestration in high-fucosylation tumours. Tumour fucosylation status defines two fundamentally distinct CRC cell states with mutually exclusive engagement of invasion programmes, metabolic pathways, immune phenotypes, and resistance mechanisms. Fucosylation represents an independent prognostic biomarker and integrative determinant of cancer cell fate, with significant implications for risk stratification and personalised therapeutic strategies. Full article
(This article belongs to the Special Issue Signaling Mechanisms Controlling Cell Fate in Cancer)
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