Overexpression of LINC00852 promotes prostate cancer cell proliferation and metastasis

Aim Long noncoding RNAs play a key role in the development and progression of various human cancers. Recently, LINC00852 has been reported to be associated with spinal metastasis lung adenocarcinoma. However, the role and potential mechanisms of LINC00852 in prostate cancer cells remain largely unknown. Methods LINC00852 expression in prostate cancer cells was examined by quantitative real-time polymerase chain reaction. Western blotting was used to detect protein expressions in prostate cancer cells. Cell cycle was analyzed by flow cytometric analysis. Cell proliferation was measured by cck-8 assay. The migration and invasion capabilities were determined using transwell assays. Results In this study, we found that LINC00852 was highly expressed in prostate cancer tissues based on the TCGA database. Overexpression of LINC00852 mediated by lentivirus significantly reinforced the proliferation and colony formation abilities of prostate cancer cell linePC3. The migration and invasion capabilities were also augmented by overexpression of LINC00852. Flow cytometric analysis revealed that LINC00852 overexpression resulted in a decrease of cells in G0/G1 phase. Moreover, overexpression of LINC00852 affected the expression of epithelial-mesenchymal transition-related proteins. Conclusions Our data collectively demonstrate that LINC00852 contributes to prostate cancer proliferation and metastasis, indicating that LINC00852is a new promising diagnostic and therapeutic target for treatment of prostate cancer.

Automated summary

In this study, it was found that LINC00852 is highly expressed in prostate cancer tissues. Overexpression of LINC00852 significantly enhanced proliferation and colony formation abilities of PC3 prostate cancer cells, as well as migration and invasion capabilities. Flow cytometric analysis showed a decrease in G0/G1 phase cells, and the expression of epithelial-mesenchymal transition-related proteins was affected by overexpression of LINC00852.