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The ceRNA network regulates epithelial-mesenchymal transition in colorectal cancer

Epithelial-mesenchymal transition (EMT) is a biological process that transforms epithelial cells into a mesenchymal phenotype, conferring cell migration and invasion capabilities. EMT is involved in the progression and metastasis of colorectal cancer (CRC). Recently, emerging evidence has shown dysr...

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Detalles Bibliográficos
Autores principales: Li, Ruina, Xu, Hui, Gao, Xiaoling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10025087/
https://www.ncbi.nlm.nih.gov/pubmed/36950593
http://dx.doi.org/10.1016/j.heliyon.2023.e14143
Descripción
Sumario:Epithelial-mesenchymal transition (EMT) is a biological process that transforms epithelial cells into a mesenchymal phenotype, conferring cell migration and invasion capabilities. EMT is involved in the progression and metastasis of colorectal cancer (CRC). Recently, emerging evidence has shown dysregulation of non-coding RNA (ncRNA) was linked to EMT. ncRNAs, including long non-coding RNA (lncRNA), regulate the transcription of downstream target genes (mRNA) through interaction with microRNAs (miRNAs); these are termed competitive endogenous RNA (ceRNA) networks. CeRNA dysregulation-induced EMT, which is linked to the progression and prognosis of CRC, has attracted wide attention. However, understanding the role of the regulation of the ceRNA network in the EMT of CRC remains limited. We discuss the molecular functions of lncRNA, the ceRNA networks related to miRNAs and mRNAs in EMT, as well as EMT transcription factors, such as the zinc finger E-box binding homeobox 1/2 (ZEB1/2), SNAIL, SLUG, and TWIST1/2. In addition, miRNAs and lncRNAs that directly target genes, thereby initiating different signaling pathways to promote EMT in CRC, were summarized. Clarifying the role of these molecules in EMT is critical for understanding molecular mechanisms and exploring the potential therapeutic targets of CRC.