Cholinergic α5 nicotinic receptor is involved in the proliferation and invasion of human prostate cancer cells.

Abstract

Nicotinic acetylcholine receptor (nAChR) subunit α5 (α5-nAChR) is involved in tumor cell proliferation, inhibition of apoptosis, progression of metastasis, and induction of angiogenesis in certain solid tumors. However, the role of α5-nAChR in prostate cancer cell growth and metastasis is unclear. In the present study, the role of α5-nAChR in cell proliferation, migration, invasion and apoptosis was investigated by silencing the expression levels of α5-nAChR in the prostate cancer cell lines DU145 and PC3. A siRNA oligonucleotide targeting α5-nAChR was designed. The cell proliferation of DU145 and PC3 cell lines was analyzed by the Cell Counting Kit-8 (CCK-8) assay. Cell migratory and invasive activities were determined using wound healing and Transwell assays, respectively. Western blot analysis was used to quantify α5-nAChR, p-AKT and p-ERK1/2 levels in DU145 and PC3 cells. Knockdown of α5-nAChR was associated with decreased cell proliferation, migration, invasion and increased apoptosis. In addition, decreased phosphorylation levels of AKT and ERK1/2 were revealed following α5-nAChR knockdown in DU145 and PC3 cells compared with those observed in the scramble control samples. The expression levels of the apoptosis-related proteins were altered following silencing of α5-nAChR. In summary, the data indicated that α5-nAChR was involved in the proliferation and invasion of human prostate cancer cells.