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Biological functions and molecular subtypes regulated by miR-142-3p in colon cancer.

Authors :
Dai L
Guo W
Xuan X
Wang B
Chai H
Yang G
Chen J
Meng X
Wang Y
Pu J
Source :
Medicine [Medicine (Baltimore)] 2023 Sep 29; Vol. 102 (39), pp. e35422.
Publication Year :
2023

Abstract

MicroRNA-142-3p (miR-142-3p) has been reported to be implicated in colon cancer; however, the possible regulatory mechanisms and molecular subtypes regulated by miR-142-3p have not been fully elucidated. This study aimed to investigate the biological functions and regulatory mechanism of miR-142-3p in colon cancer. The expression level of miR-142-3p in colon cancer was analyzed based on the mRNA and miRNA expression datasets of colon cancer retrieved from The Cancer Genome Atlas. Target genes of miR-142-3p were also predicted. Based on these target genes, the functions and subtypes of miR-142-3p were investigated. The metabolic and tumor-related pathways, immune microenvironment, and target gene expression between the 2 subtypes were analyzed. MiR-142-3p was upregulated in tumor tissues, and its high expression indicated a poor prognosis. A total of 39 target genes were predicted, which were significantly involved in autophagy- and metabolism-related functions and pathways. Based on these target genes, the colon cancer samples were clustered into 2 subtypes. There were 35 metabolism-related pathways that were significantly different between the 2 clusters. The immune and stromal scores in cluster 2 were higher than those in cluster 1, whereas the tumor purity of cluster 2 was significantly lower than that of cluster 1. TP53INP2 expression in cluster 2 was higher than that in cluster 1. MiR-142-3p may promote colon cancer progression via autophagy- and metabolism-related pathways. MiR-142-3p may be served as a candidate target for the treatment of colon cancer.<br />Competing Interests: The authors have no conflicts of interest to disclose.<br /> (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Details

Language :
English
ISSN :
1536-5964
Volume :
102
Issue :
39
Database :
MEDLINE
Journal :
Medicine
Publication Type :
Academic Journal
Accession number :
37773805
Full Text :
https://doi.org/10.1097/MD.0000000000035422