P53 Regulation-Association Long Non-Coding RNA (LncRNA PRAL) Inhibits Cell Proliferation by Regulation of P53 in Human Lung Cancer

BACKGROUND Lung cancer is among the most common causes of cancer-related deaths worldwide, but its tumorigenic mechanisms are largely unknown. Long non-coding RNAs (LncRNAs) have been shown to have significant roles in multiple cancers. Herein, we aimed to elucidate the detailed effects of a newly-discovered LncRNA, termed PRAL, on cell proliferation in lung cancer. MATERIAL AND METHODS A total of 100 lung cancer patients were subjected to RT-PCR analysis to detect the expressions of PRAL. Western blot analysis was performed to examine P53 protein levels. PRAL plasmid and specific siRNA against P53 was transfected into lung cancer cell lines NCI-H929 and A549. Cell viability assay was conducted in the presence or absence of siP53. RESULTS The transcript level of PRAL in human lung cancer was remarkably decreased in vivo compared with their adjacent non-cancerous counterparts, and the protein levels of P53 were accordingly suppressed. Moreover, the expression of PRAL was also decreased in all of the 5 lung cancer cell lines. Transfection of PRAL plasmid inhibited cell proliferation in NCI-H929 and A549 cells and promoted the transcription of P53; however, knockdown of P53 caused no notable effects on PRAL transcription, but it retarded the inhibitory effects mediated by PRAL. CONCLUSIONS The transcript level of PRAL was decreased in lung cancer in vivo and in vitro. Overexpression of PRAL inhibited cell proliferation by upregulating the expression of P53. Our results indicate that PRAL might be a tumor suppressor in lung cancer and thus provides novel clues for the diagnosis and treatment for lung cancer in clinical practice.