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Abstract

Volume 17, Issue 5 (September 2015) 17, 850–853; doi: 10.4103/1008-682X.142134

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

Wei Liu1,2,*, Bo Kou1,2,*, Zhen‑Kun Ma1,2, Xiao‑Shuang Tang1,2, Chuan Lv3, Min Ye4, Jia‑Qi Chen1,2, Lei Li1, Xin‑Yang Wang2, Da‑Lin He1,2

Wei Liu1,2,*, Bo Kou1,2,*, Zhen‑Kun Ma1,2, Xiao‑Shuang Tang1,2, Chuan Lv3, Min Ye4, Jia‑Qi Chen1,2, Lei Li1, Xin‑Yang Wang2, Da‑Lin He1,2

Correspondence: Correspondence: Dr. DL He (hedl@mail.xjtu.edu.cn)

2015-2-6

Abstract

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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Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.