Long noncoding RNA TNFRSF10A-AS1 promotes colorectal cancer through upregulation of HuR

BACKGROUND 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. AIM To explore the functional role and underlying molecular mechanisms of lncRNA TNFRSF10A-AS1 in CRC. METHODS 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. RESULTS 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. CONCLUSION 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.

Automated summary

Recent studies have identified TNFRSF10A-AS1 as a highly expressed long noncoding RNA in colorectal cancer (CRC). It has been found that TNFRSF10A-AS1 promotes CRC tumorigenesis and progression by acting as a molecular sponge for miR-3121-3p and regulating HuR expression. These findings suggest that TNFRSF10A-AS1 could be a potential therapeutic target for CRC.