Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma

  • Authors:
    • Juan Wang
    • Zhihong Ai
    • Jing Chen
    • Yincheng Teng
    • Jieping Zhu
  • View Affiliations

  • Published online on: April 17, 2018     https://doi.org/10.3892/ol.2018.8518
  • Pages: 9429-9435
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Endometrial carcinoma is the most common gynecological malignancy of the female genital tract worldwide (2012). Enhancer of zeste homolog 2 (EZH2), a critical component of the polycomb repressive complex 2, has been found to be associated with multiple biological processes and is overexpressed in multiple types of cancer. Previous studies have demonstrated that EZH2 is associated with endometrial carcinoma. The present study investigated the expression and biology function of EZH2 in endometrial cancer (EC). It was found that EZH2 levels were markedly increased in endometrial cancer tissues compared with that in adjacent normal tissues. EZH2 was significantly overexpressed in 3 separate endometrial cancer cell lines (Ishikawa, RL95‑2 and HEC1‑A) when compared with the normal endometrial cell line ESC. Additionally, small interfering RNA was used to investigate the role of EZH2 in endometrial carcinoma cell proliferation, and the results showed that EZH2 knockdown suppressed the proliferation of endometrial carcinoma cells in vitro. Furthermore, EZH2 knockdown induced apoptosis of human EC cells by promoting the expression of pro‑apoptosis protein caspase 3, caspase 9, BCL2 associated X and decreasing the expression of anti‑apoptosis protein Bcl‑2. Finally, the present study demonstrated that EZH2 knockdown suppressed the invasion of EC cells through downregulation of the epithelial‑mesenchymal transition. Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.
View Figures
View References

Related Articles

Journal Cover

June-2018
Volume 15 Issue 6

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Wang J, Ai Z, Chen J, Teng Y and Zhu J: Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma. Oncol Lett 15: 9429-9435, 2018.
APA
Wang, J., Ai, Z., Chen, J., Teng, Y., & Zhu, J. (2018). Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma. Oncology Letters, 15, 9429-9435. https://doi.org/10.3892/ol.2018.8518
MLA
Wang, J., Ai, Z., Chen, J., Teng, Y., Zhu, J."Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma". Oncology Letters 15.6 (2018): 9429-9435.
Chicago
Wang, J., Ai, Z., Chen, J., Teng, Y., Zhu, J."Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma". Oncology Letters 15, no. 6 (2018): 9429-9435. https://doi.org/10.3892/ol.2018.8518