ORIGINAL ARTICLE
Year : 2015  |  Volume : 17  |  Issue : 5  |  Page : 850-853

Tetrandrine suppresses proliferation, induces apoptosis, and inhibits migration and invasion in human prostate cancer cells


1 Department of Urology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University; Oncology Research Lab, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of the People's Republic of China, Xi'an, 710061, China
2 Department of Urology, First People's Hospital of Jining, Jining, 272100, China
3 Ophthalmology department, The First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, 710061, China
4 Department of Urology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, 710061, China
5 Oncology Research Lab, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of the People's Republic of China, Xi'an, 710061, China

Correspondence Address:
Da-Lin He
Department of Urology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University; Oncology Research Lab, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of the People's Republic of China, Xi'an, 710061
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1008-682X.142134

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Tetrandrine (TET), a traditional Chinese medicine, exerts remarkable anticancer activity on various cancer cells. However, little is known about the effect of TET on human prostate cancer cells, and the mechanism of function of TET on prostate cancer has not yet been elucidated. To investigate the effects of TET on the suppression of proliferation, induction of apoptosis, and inhibition of migration and invasion in human prostate cancer cell lines, DU145 and PC-3. Inhibition of growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and clone formation assay, and flow cytometry analysis was performed to detect the induction of apoptosis. Activation of poly (ADP-ribose) polymerase, caspase-3, Akt, phospho-Akt, Bcl-2, and Bax was analyzed by Western blotting. Wound healing assay and transwell migration assay were used to evaluate the effect of TET on migration and invasion of cancer cells. TET inhibited the growth of DU145 and PC-3 cells in a dose- and time-dependent manner. Cell cloning was inhibited in the presence of TET in DU145 and PC-3 cells. TET suppressed the migration of DU145 and PC-3 cells. Transwell invasion assay showed that TET significantly weakened invasion capacity of DU145 and PC-3 cells. TET exhibited strong inhibitory effect on proliferation, migration, and invasion of prostate cancer cells. In addition, TET induced apoptosis in a dose-dependent manner by activating the caspase cascade and inhibiting phosphoinositide 3-kinase-Akt signal pathway. The accumulating evidence suggests that TET could be a potential therapeutic candidate against prostate cancer in a clinical setting.


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