Daidzein inhibits choriocarcinoma proliferation by arresting cell cycle at G1 phase through suppressing ERK pathway in vitro and in vivo

Oncol Rep. 2017 Oct;38(4):2518-2524. doi: 10.3892/or.2017.5928. Epub 2017 Aug 28.

Abstract

Choriocarcinoma is a highly malignant tumor arising from abnormal gestational trophoblast proliferation. Although chemotherapy has dramatically improved the prognosis, there are still some patients who become drug-resistant or relapse. Daidzein has garnered interest in its antitumor activity especially in proliferation inhibition. However, few reports exist on daidzein effect in growth of choriocarcinoma. Therefore, in this study, we performed in vitro and in vivo experiment in JAR and JEG‑3 to investigate the effect of daidzein in proliferation of choriocarcinoma. Daidzein inhibited cell growth in a time- and dose-dependent way. Cell cycle was arrested at G1 phase and expression of cyclin D1, c-myc, PCNA was reduced while p21 was upregulated during daidzein treatment. At the same time, the expression of p-ERK was downregulated and translocation into nuclear afterwards was also inhibited. Moreover, ERK agonist ceramide C6 abolished daidzein's effects on cell proliferation. Besides, in vivo experiment also showed daidzein's anti-proliferation function as xenografts growth was inhibited and expressions of c-myc, PCNA and p-ERK were suppressed. In conclusion, results in our study demonstrate daidzein can inhibit choriocarcinoma cell proliferation in vitro and in vivo; underlying mechanism behind the inhibitory effects may probably be suppressing ERK pathway and afterwards arresting cell cycle at G1 phase.

MeSH terms

  • Animals
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Choriocarcinoma / drug therapy*
  • Choriocarcinoma / genetics
  • Choriocarcinoma / pathology
  • G1 Phase / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Isoflavones / administration & dosage*
  • MAP Kinase Signaling System / drug effects
  • Mice
  • Neoplasm Proteins / genetics*
  • Neoplasm Recurrence, Local / drug therapy*
  • Neoplasm Recurrence, Local / genetics
  • Neoplasm Recurrence, Local / pathology
  • Phosphorylation
  • Xenograft Model Antitumor Assays

Substances

  • Isoflavones
  • Neoplasm Proteins
  • daidzein