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

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.

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