Prostate cancer is a common multiple malignant tumor occurring in males. Prostate cancer mortality is the 2nd most common of all tumor types in Western countries and the mortality of morbidity is 13% in the USA. The present study aimed to investigate the anticancer effect of docetaxel on inducing the apoptosis of prostate cancer via the cofilin‑1 and paxillin signaling pathway. Treatment with docetaxel (1‑50 nM) disposed the human LNCaP prostate cancer cells for 24 h. Cell growth and cytotoxicity were subsequently measured using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase assay, respectively. Docetaxel-induced cell death was analyzed using flow cytometric and caspase-3 assays. Reverse transcription‑quantitative polymerase chain reaction analysis was used to detect the gene expression of cofilin‑1 and western blots were used to determine the protein expression of paxillin. Treatment with docetaxel inhibited cell growth, promoted cytotoxicity, activated apoptosis and increased caspase‑3 activity in the LNCaP cells. Notably, administration of docetaxel reduced the gene expression of cofilin‑1 and the protein expression of paxillin in the LNCaP cells. Additionally, knockdown of cofilin‑1 advanced the anticancer effect of docetaxel against LNCaP cells through suppression of the paxillin pathway. The present findings demonstrated that the anticancer effect of docetaxel induces the apoptosis of prostate cancer via the suppression of the cofilin‑1 and paxillin signaling pathways, which will assist in setting a stage for the clinical treatment of prostate cancer.

Objectives: Docetaxel was the first drug with proven survival benefit in men with castration-resistant prostate cancer. Acquired resistance to docetaxel precedes fatality in castration-resistant prostate cancer. The aims of this study were to evaluate docetaxel-sensitive and docetaxel-resistant proteomes in PC-3 cells, and to investigate the molecular mechanism of docetaxel-resistant PC-3 cells. Methods: Docetaxel-resistant PC-3 cells were developed by docetaxel dose escalation. The global profiling of the protein expression was investigated in docetaxel-sensitive and docetaxel-resistant proteomes in PC-3 cells using 2-dimensional polyacrylamide gel electrophoresis/matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Results: Forty-nine differential proteins were found in docetaxel-resistant PC-3 cells in comparison with docetaxel-sensitive PC-3 cells. Expression in 29 proteins was upregulated, whereas expression in 20 proteins was downregulated. ATP synthase and galectin-1 were involved in the formation of tumor vessels; calreticulin, cathepsin D, and cofilin were involved in tumor metastasis, and GRP78 (78-kDa glucose-regulated protein) and microtubule-associated protein-6 were involved in drug resistance of tumor. Conclusion: It is suggested that a proteomic expression difference exists between docetaxel-sensitive and docetaxel-resistant PC-3 cells, which would be helpful for further understanding the molecular mechanisms of docetaxel resistance in PC-3 cells.