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

{"title":"Wnt/β-catenin pathway as a link between therapy resistance-driven epithelial-mesenchymal transition and stemness in colorectal cancer","authors":"Murilo Ramos Rocha, Yuri Kelly Castillo-Medina, Bárbara Martins de Lima Coelho, Luidy Lucas Lopes Rios, Jose Andres Morgado-Diaz","doi":"10.1002/cbin.12270","DOIUrl":null,"url":null,"abstract":"<p>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.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"154-160"},"PeriodicalIF":3.3000,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology International","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cbin.12270","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

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.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

Wnt/β-catenin通路在治疗耐药驱动的结直肠癌上皮-间质转化和干细胞之间的联系

经历上皮-间质转化（EMT）的细胞的高可塑性促进了肿瘤异质性的增加，其与肿瘤相关基质细胞的相互作用似乎有助于形成干性表型。具有这些特征的细胞对化疗和放疗的抵抗力增加，导致疾病复发和转移。在这里，我们讨论了Wnt/β-catenin通路在细胞对这些疗法产生耐药性的背景下促进EMT和干细胞的激活。我们讨论EMT和癌症干细胞（CSCs）是否共同或独立发挥作用，或者它们的发育是否存在联系。我们进一步提出，这一途径对于建立这两种表型之间的联系是必要的。并表明，当抑制时，它可能会阻碍治疗诱导的EMT细胞中CSCs的增加。了解这种细胞现象可能有助于开发新的靶向治疗方法，以改善临床反应，特别是在结直肠癌中。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

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.