Tetrandrine suppresses cervical cancer growth by inducing apoptosis in vitro and in vivo
Authors Zhang H, Xie B, Zhang Z, Sheng X, Zhang S
Received 16 September 2018
Accepted for publication 5 November 2018
Published 20 December 2018 Volume 2019:13 Pages 119—127
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 2
Editor who approved publication: Dr Tuo Deng
Haiyan Zhang,1,2 Beibei Xie,2 Zhen Zhang,2 Xiugui Sheng,3 Shiqian Zhang1
1Department of Gynecology, Affiliated Qilu Hospital of Shandong University, Linyi, People’s Republic of China; 2Department of Gynecology Ward-1, Linyi City People’s Hospital, Linyi, People’s Republic of China; 3Department of Gynecology, Cancer Hospital Chinese Academy of Medical Sciences, Beijing, People’s Republic of China
Introduction and aim: Cervical cancers are the most common forms of cancer that occur in women globally and are difficult to be cured in their terminal stages. Tetrandrine (TET), a monomeric compound isolated from a traditional Chinese medicine, Radix Stephania tetrandrae, exhibits anticancer effects on different tumor types. However, the mechanisms by which TET regulates the proliferation, apoptosis, migration, and invasion in cervical cancer remain unclear. Thus, this study aimed to investigate the therapeutic effects of TET on cervical cancer in vitro and in vivo.
Methods: Cell Counting Kit-8, immunofluorescence, flow cytometry, wound healing, and transwell migration assays were used to detect cell proliferation, apoptosis, and migration and invasion, respectively, in vitro. In addition, immunohistochemical assays were performed to evaluate tumor growth and apoptosis in vivo. Moreover, Western blotting was used to examine active caspase 3, matrix metalloproteinase (MMP)2, and MMP9 protein levels in vitro and in vivo.
Results: The results revealed that TET significantly inhibited SiHa cell proliferation in vitro and suppressed tumor growth in vivo. Meanwhile, TET was revealed to induce cervical cancer cell apoptosis by upregulating active caspase 3 in vitro and in vivo. Furthermore, the migration and invasion of SiHa cells were inhibited by TET accompanied with MMP2 and MMP9 downregulation.
Conclusion: We have shown that TET inhibited cervical tumor growth and migration in vitro and in vivo for the first time. The accumulating evidence suggests that TET could be a potential therapeutic agent for the treatment of cervical cancer.
Keywords: tetrandrine, cervical cancer, proliferation, apoptosis, migration
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