Insights into the molecular mechanisms and signalling pathways of epithelial to mesenchymal transition (EMT) in colorectal cancer: A systematic review and bioinformatic analysis of gene expression

• Main Authors: Azizan, Suha, Cheng, Kim Jun, Mohamed, Elsa Haniffah Mejia, Ibrahim, Kamariah, Faruqu, Farid Nazer, Vellasamy, Kumutha Malar, Khong, Tak Loon, Syafruddin, Saiful Effendi, Ibrahim, Zaridatul Aini
• Format: Article
• Published: ELSEVIER 2024
• Subjects: RC0254 Neoplasms. Tumors. Oncology (including Cancer); Z Bibliography. Library Science. Information Resources
• Online Access: http://eprints.um.edu.my/44248/; https://doi.org/10.1016/j.gene.2023.148057
• Institution: Universiti Malaya

Colorectal cancer (CRC) is ranked as the second leading cause of mortality worldwide, mainly due to metastasis. Epithelial to mesenchymal transition (EMT) is a complex cellular process that drives CRC metastasis, regulated by changes in EMT-associated gene expression. However, while numerous genes have been identified as EMT regulators through various in vivo and in vitro studies, little is known about the genes that are differentially expressed in CRC tumour tissue and their signalling pathway in regulating EMT. Using an integration of sys-tematic search and bioinformatic analysis, gene expression profiles of CRC tumour tissues were compared to non-tumour adjacent tissues to identify differentially expressed genes (DEGs), followed by performing systematic review on common identified DEGs. Fifty-eight common DEGs were identified from the analysis of 82 tumour tissue samples obtained from four gene expression datasets (NCBI GEO). These DEGS were then systematically searched for their roles in modulating EMT in CRC based on previously published studies. Following this, 10 common DEGs (CXCL1, CXCL8, MMP1, MMP3, MMP7, TACSTD2, VIP, HPGD, ABCG2, CLCA4) were included in this study and subsequently subjected to further bioinformatic analysis. Their roles and functions in modulating EMT in CRC were discussed in this review. This study enhances our understanding of the molecular mechanisms underlying EMT and uncovers potential candidate genes and pathways that could be targeted in CRC.