Published online May 28, 2022. doi: 10.3748/wjg.v28.i20.2184
Peer-review started: October 26, 2021
First decision: December 27, 2021
Revised: January 10, 2022
Accepted: April 20, 2022
Article in press: April 20, 2022
Published online: May 28, 2022
Processing time: 213 Days and 4.3 Hours
Recent studies have emphasized the emerging importance of long noncoding RNAs (lncRNAs) in colorectal cancer (CRC). However, the functions and regulatory mechanisms of numerous lncRNAs in CRC have not been fully elucidated.
To explore the functional role and underlying molecular mechanisms of lncRNA TNFRSF10A-AS1 in CRC.
TNFRSF10A-AS1 expression was measured by quantitative real-time polymerase chain reaction in CRC, and the relationship between TNFRSF10A-AS1 levels and the clinicopathological features of CRC patients was analyzed. The effect of TNFRSF10A-AS1 expression on CRC proliferation and metastasis was examined in vitro and in vivo. Mechanistically, we investigated how TNFRSF10A-AS1 is involved in CRC as a competitive endogenous RNA.
TNFRSF10A-AS1 was expressed at a high level in CRC and the upregulation of TNFRSF10A-AS1 was associated with advanced T grade and tumor size in CRC patients. A functional investigation revealed that TNFRSF10A-AS1 enhanced the proliferation, migration ability and invasion ability of colon cancer cells in vitro and in vivo. A mechanistic analysis demonstrated that TNFRSF10A-AS1 acted as a miR-3121-3p molecular sponge to regulate HuR expression, ultimately promoting colorectal tumorigenesis and progression.
TNFRSF10A-AS1 exerts a tumor-promoting function through the miR-3121-3p/HuR axis in CRC, indicating that it may be a novel target for CRC therapy.
Core Tip: TNFRSF10A-AS1 was upregulated in colorectal cancer (CRC) tumor tissues and cell lines, and it was positively correlated with tumor grade and size in patients with CRC. In addition, TNFRSF10A-AS1 facilitated CRC growth and metastasis. Mechanistically, TNFRSF10A-AS1 was predominantly found in the cytoplasm of CRC cell lines and upregulated the level of the downstream target, HuR, by sponging miR-3121-3p, thereby further promoting colorectal tumorigenesis and progression.