LINC00152 promotes hepatocellular carcinoma progression by regulating PI3k/Akt/mTOR signaling pathway through miR-139/PIK3CA
Menée à l'aide de lignées cellulaires et d'échantillons tissulaires de carcinomes hépatocellulaires, cette étude met en évidence un mécanisme par lequel le long ARN non codant LINC00152 favorise la progression tumorale en régulant la voie de signalisation PI3k/Akt/mTOR via le microARN miR-139 et la protéine PIK3CA
Hepatocellular carcinoma (HCC) ranks as the fifth most common cancer worldwide, and is the primary histological subtype of liver cancer with high incidence and poor prognosis. Recently, numerous long non-coding RNAs (lncRNAs) have been reported to be associated with the tumorigenesis of HCC, however, the underlying mechanisms of LINC00152 action in HCC are poorly understood. Herein, we identified a significant up-regulation of LINC00152 both in HCC tissues and cell lines. Functional studies showed that knockdown of LINC00152 inhibited cell proliferation, migration, and invasion, but promoted cell apoptosis, indicating its oncogenic functions in HCC tumorigenesis. Mechanistically, LINC00152 functioned as an efficient miR-139 sponge, thereby released the suppression of PIK3CA (a target gene of miR-139). Anti-miR-139 rescued the inhibition of cell proliferation, migration, and invasion induced by LINC00152 knockdown. Similarly, PIK3CA overexpressing plasmid also reversed miR-139–mediated biological functions in HCC cells. Taken together, our study revealed a crucial regulatory network of LINC00152/miR-139/PIK3CA axis in the tumorigenesis of HCC, implying that LINC00152 may be a biomarker and novel therapeutic target for further clinical therapy of HCC.