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Purified Vitexin Compound 1 Suppresses Tumor Growth and Induces Cell Apoptosis in a Mouse Model of Human Choriocarcinoma
  1. Zhihui Tan, MD*,
  2. Yi Zhang, PhD*,
  3. Jun Deng, MD*,
  4. Guangyao Zeng, PhD and
  5. Yu Zhang, PhD*
  1. * Department of Obstetrics and Gynecology, Xiangya Hospital, Central South University, and
  2. College of Pharmacy, Central South University, Changsha, Hunan, People’s Republic of China.
  1. Address correspondence and reprint requests to Yi Zhang, PhD, Department of Obstetrics and Gynecology, Xiangya Hospital, Central South University Changsha, Hunan, People’s Republic of China, 87 Xiangya Rd, Changsha, Hunan, China. E-mail: zhangyitanzhihui{at}yahoo.com.cn.

Abstract

Objective In our previous study, we had isolated a series of lignan compounds, termed vitexins, from the seed of Chinese herb Vitex negundo and found broad antitumor activities of these compounds in many cancer xenograft models and cell lines. This study was aimed to determine the antitumor effect of purified vitexin compound 1 (VB1) on choriocarcinoma in vitro and in vivo.

Materials and Methods The severe combined immunodeficiency mouse model of choriocarcinoma was established to investigate the in vivo effect of VB1. Its effect on proliferation and apoptosis in JEG-3 cell line was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay and flow cytometry, respectively. The expression of caspase-3, Bcl-2, and some molecules involved in the mammalian target of rapamycin (mTOR) signaling was detected by Western blot.

Results Vitexin compound 1 significantly inhibited the growth of choriocarcinoma in severe combined immunodeficient mice and reduced the serum β-human chorionic gonadotropin level. Vitexin compound 1 inhibited cell proliferation, induced apoptosis, and inhibited the mTOR signaling in JEG-3 cell line.

Conclusion Vitexin compound 1 could inhibit choriocarcinoma via inducing cell apoptosis and suppressing the mTOR pathway.

  • Vitexin
  • Choriocarcinoma
  • Apoptosis
  • mTOR signaling

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Footnotes

  • The authors declare that there are no conflicts of interest.

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