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SUMO-1 Promotes Ishikawa Cell Proliferation and Apoptosis in Endometrial Cancer by Increasing Sumoylation of Histone H4
  1. Jindan Zheng, GG,
  2. Lili Liu, MM,
  3. Shanfeng Wang, MM and
  4. Xin Huang, MM
  1. Department of Obstetrics and Gynecology, First Affiliated Hospital, Liaoning Medical College, Jinzhou, Liaoning, China.
  1. Address correspondence and reprint requests to Lili Liu, MM, Department of Obstetrics and Gynecology, First Affiliated Hospital of Liaoning Medical College, No. 2, Section 5, Renmin St, Jinzhou City, Liaoning Province 210700, China. E-mail:


Objectives To investigate the functional role of SUMO-1 on cell proliferation and apoptosis in endometrial cancer cells (Ishikawa line) and to explore the underlying regulatory mechanisms.

Methods Different concentrations of estradiol (E2) and small interfering RNA (siRNA) targeting the SUMO-1 (siCo) were treated in Ishikawa cells, and then quantitative polymerase chain reaction was used to examine the expression of progesterone receptor (PR) expression in Ishikawa cells. Western blots were applied to validate histone H4 sumoylation. CCK8 assay and flow cytometry were performed to investigate cell proliferation and apoptosis in Ishikawa cells.

Results Estradiol up-regulated the expression of PR messenger RNA, most obviously at 100 nM. SUMO-1 siRNA decreased the PR expression. Estradiol up-regulated H4 sumoylation and caused the increase of Ishikawa cell proliferation, whereas SUMO-1 siRNA down-regulated H4 sumoylation, inhibited the cell proliferation, and induced apoptosis. Furthermore, SUMO-1 siRNA-transfected cells were arrested in the S and G2/M phases and E2 increased the S and G2/M phases of Ishikawa cells.

Conclusion SUMO-1 regulates the Ishikawa cell proliferation and apoptosis by the sumoylation of histone H4.

  • SUMO-1
  • Histone H4 sumoylation
  • Endometrial cancer cells
  • Proliferation
  • Apoptosis

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  • Funding: Our work was funded by Liaoning Natural Science (201102134).

  • The authors declare no conflicts of interest.