Long non-coding RNA TDRG1 aggravates colorectal cancer stemness by binding with miR-873-5p to upregulate PRKAR2.

Environ Toxicol

Department of Gastrointestinal oncology Surgery, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, P. R. China. The School of Clinical Medicine, Fujian Medical University. The Graduate School of Fujian Medical University, Xiamen, China.

Published: October 2022

The effects of long non-coding RNA TDRG1 have been established in several tumors; however, its roles in colorectal cancer (CRC) progression are never been found. Here, we found that TDRG1 level was upregulated in CRC cells compared to that in normal colon epithelial cells. Additionally, TDRG1 level was remarkably upregulated in 3D non-adherent spheres derived from the parental CRC cells. Further in vitro and in vivo revealed that TDRG1 knockdown suppressed the stemness of CRC cells. What's more, combined with bioinformatics analysis, luciferase reporter and RNA pull down experiments showed that TDRG1 could bind to miR-873-5p, downregulated its level and thus increase the expression of PRKAR2. Finally, it was shown that TDRG1 functioned through the miR-873-5p/PRKAR2 axis. This study demonstrated a novel TDRG1/miR-873-5p/PRKAR2 signaling in CRC progression.

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http://dx.doi.org/10.1002/tox.23602DOI Listing

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