Wnt/β-catenin pathway as a link between therapy resistance-driven epithelial-mesenchymal transition and stemness in colorectal cancer.

IF 3.3 3区生物学 Q3 CELL BIOLOGY Cell Biology International Pub Date : 2024-12-20 DOI:10.1002/cbin.12270

Murilo Ramos Rocha, Yuri Kelly Castillo-Medina, Bárbara Martins de Lima Coelho, Luidy Lucas Lopes Rios, Jose Andres Morgado-Diaz

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引用次数: 0

Abstract

The high plasticity of cells undergoing epithelial-mesenchymal transition (EMT) promotes increased tumor heterogeneity, and its interaction with tumor-associated stromal cells appears to contribute to developing a stemness phenotype. Cells with these characteristics exhibit increased resistance to chemotherapy and radiotherapy, leading to disease relapse and metastasis. Here, we discuss the activation of the Wnt/β-catenin pathway in promoting EMT and stemness within the context of cellular resistance to these therapies. We discuss whether EMT and cancer stem cells (CSCs) function in conjunction, independently, or if a link is connecting their development. We further propose that this pathway is necessary to establish a connection between these two phenotypes. And suggest that it could hinder the rise of CSCs from treatment-induced EMT cells when inhibited. Understanding this cellular phenomenon might allow the development of new targeted therapies to improve clinical responses, particularly in colorectal cancer.

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来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.