PRKACB is downregulated in non-small cell lung cancer and exogenous PRKACB inhibits proliferation and invasion of LTEP-A2 cells

Protein kinase cAMP-dependent catalytic beta (PRKACB) is a member of the Ser/Thr protein kinase family and a key effector of the cAMP/PKA-induced signal transduction involved in numerous cellular process, including cell proliferation, apoptosis, gene transcription, metabolism and differentiation. In the present study, the expression pattern of PRKACB in non-small cell lung cancer (NSCLC) and the effect of PRKACB upregulation on cell proliferation, apoptosis and invasion were investigated. PRKACB mRNA and protein expression was analyzed in the NSCLC tissue and corresponding normal tissues of 30 cases, using quantitative RT-PCR and western blot analysis. A plasmid containing full-length PRKACB was transfected into LTEP-A2 cells to further investigate the effects of PRKACB overexpression on proliferation, apoptosis and invasion of the transfected cells, which were examined using 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltet-razolium bromide (MTT), colony formation, flow cytometry and Transwell assays. The results revealed that the NSCLC tissues exhibited much lower levels of PRKACB mRNA and protein compared with their corresponding normal tissues. The upregulation of PRKACB decreased the numbers of proliferative, colony and invasive cells, while the apoptotic rates of transfected cells were increased. These data indicate that PRKACB is downregulated in NSCLC tissues and that upregulation of PRKACB may be an effective way to prevent the progression of NSCLC.