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

Abstract

Protein kinase cAMP-dependent catalytic β (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-diphenyltetrazolium 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.

Role of Circular RNA DLEU2 in Human Acute Myeloid Leukemia

“…The PRKACB gene encodes cAMP-dependent protein kinase A (PKA) catalytic subunit ␤ and is located on chromosome 1p31.1 (22). The PRKACB protein belongs to the Ser/Thr protein kinase family and is a pivotal modulator of the cAMP/PKA pathway, which is intimately correlated with a host of cellular processes, including cell reproduction, gene transcription, and metabolism (23).…”

A novel prognostic factor TRIM44 promotes cell proliferation and migration, and inhibits apoptosis in testicular germ cell tumor

“…In contrast, neither of these reported pathways was associated with TRIM44. Interestingly, microarray analysis showed that nine out of top 20 downregulated genes had oncogenic function ( C3AR1, FMN1, GBP1, ST3GAL5, NT5E, RAB27B, FBP2, HIPK3, PLAU , and 8 out of 20 top up‐regulated genes had tumor suppressive function ( NUPR1, CDK19, CADM1, INHBA, TNFSF10, PRKACB, PCDHB6, DDIT4 ). Furthermore, six of these eight tumor suppressive genes are associated with apoptotic mechanisms ( NUPR1 , CDK19, CADM1, INHBA, TNFSF10, DDIT4 ).…”

Activating PRKACB somatic mutation in cortisol-producing adenomas

“…Cβ-knockout mouse models suggest distinct roles for Cβ and Cα in neuronal development and hippocampal plasticity (14,15). An involvement of Cβ in cancer has been demonstrated, with studies indicating that Cβ is playing either a role as a tumor suppressor gene (16) or as an oncogene (17,18), depending on the cell model tested. It has been suggested that upregulation of PRKACB is critical for c-MYC-associated tumorigenesis (17,19).…”