The long noncoding RNA RMRP-miR-3135a-SV2A axis promotes the development of hepatocellular carcinoma

Long noncoding RNA (lncRNA) RMRP has been associated with the progression of hepatocellular carcinoma (HCC), but its specific role and underlying mechanisms remain unclear. This study aimed to characterize the function of lncRNA RMRP in HCC and determine its potential as a therapeutic target.

We examined the expression of lncRNA RMRP in HCC tissues and normal tissues. Knockdown experiments were conducted using lentiviruses targeting lncRNA RMRP in HCC cell lines. Cell proliferation, apoptosis, and migration assays were performed to assess the effects of lncRNA RMRP knockdown. Mechanistic studies were conducted to clarify the regulatory relationship between lncRNA RMRP, miR-3135a, and SV2A. Functional rescue experiments and in vivo mouse xenograft models were also employed to validate the findings.

Our results demonstrated that lncRNA RMRP is upregulated in HCC tissues compared to normal tissues. Knockdown of lncRNA RMRP in HCC cell lines resulted in suppressed cell proliferation, increased apoptosis, and reduced migration. Mechanistic investigations revealed that lncRNA RMRP regulates SV2A expression by sponging miR-3135a to regulate HCC development. Notably, lncRNA RMRP also possessed positive correlations with several immune checkpoints. In vivo studies using a mouse xenograft model confirmed that lncRNA RMRP knockdown significantly inhibits tumor growth.

The lncRNA RMRP-miR-3135a-SV2A axis may be a key contributor to HCC progression. The study's findings provide insights into the molecular mechanisms of HCC and support the lncRNA RMRP-miR-3135a-SV2A axis as a potential therapeutic target, offering promising avenues for developing novel HCC treatments.