Lung adenocarcinomas have increased RMRP expression, which is associated with poor prognosis. ALKBH5 upregulates RMRP expression via demethylation, indicating that targeting RMRP through ALKBH5 manipulation could be a promising therapeutic strategy for lung adenocarcinoma.
Lung adenocarcinomas are more common in non-smoking males and females. In this study, we investigated the function of long non-coding RNA RMRP in lung adenocarcinoma and further explore the regulatory role of ALKBH5 in lncRNA methylation. The results showed lncRNA RMRP expression was significantly enhanced in lung adenocarcinoma tissues, and is positively correlated with poor prognosis. RMRP knockdown in lung adenocarcinoma cell lines suppressed cell proliferation, migration and invasion, and promoted cell apoptosis. In addition, ALKBH5 upregulated RMRP expression via demethylation, and ALKBH5 knockdown inhibited the tumorigenesis of lung adenocarcinoma in vitro and vivo. Given these clear patterns, suppressing RMRP through ALKBH5 manipulation may represent a promising therapeutic target for lung adenocarcinoma.
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