Long Non-Coding RNA SNHG12 Promotes Prostate Tumor Occurrence and Progression via AKT Regulation

Abstract BackgroundIncreasing studies have shown that long noncoding RNAs (lncRNAs) participated in the development of prostate cancer (PCa). The small nucleolar RNA host gene 12 (SNHG12) has been reported to play an important role in the tumorigenesis and progression of PCa, but the functional underlying mechanism has not been studied clearly. MethodsWe detected the expression level of SNHG12 in PCa tissues and matched adjacent normal tissues that were collected from 85 patients. Then, colony formation assays, MTT experiments and flow cytometry were used to examine the effect of SNHG12 on proliferation, cell cycle distribution and apoptosis of DU145 cells. Further, Transwell invasion assay was utilized to assess whether SNHG12 participates in PCa cell invasion and affects the secretion of VEGF secretion in DU145 cells. Western blot analysis was applied to quantify the expression level of apoptosis-related and invasion-related proteins. Finally, we investigated the effect of SNHG12 on tumor growth in vivo. ResultsWe found that SNHG12 expression was upregulated in prostate tumor tissues compared with the matched adjacent normal tissues. SNHG12 knockdown increased the expression of apoptosis-related protein Caspase 3, whereas downregulated the expression of MMP9, which is an invasion-related protein. SNHG12 knockdown inhibited the expression of phosphorylated AKT. In vivo xenograft experiments showed that knockdown of SNHG12 suppressed the PCa growth. ConclusionsThe above-mentioned results revealed that SNHG12 promoted cell proliferation and suppressed apoptosis in PCa cells, which suggests that SNHG12 is probably a novel PCa biomarker and therapy target of PCa.