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S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member IInduced Human Ovarian Cancer SKOV3 Cell Lines

Zhu, Qiaoying MD*†; Hu, Jianming MD; Meng, Huijuan MD; Shen, Yufei MD*†; Zhou, Jinhua MD; Zhu, Zhihong MD

International Journal of Gynecological Cancer: May 2014 - Volume 24 - Issue 4 - p 629–634
doi: 10.1097/IGC.0000000000000105
Basic Science

Objective: Aplasia Ras homolog member I (ARHI) is associated with human ovarian cancer (HOC) growth and proliferation; however, the mechanisms are unclear. The purpose of this study was to investigate ARHI effects in HOC SKOV3 cells.

Methods: We transfected SKOV3 cells with PIRES2-EGFP-ARHI and measured growth inhibition rates, cell cycle distribution, apoptosis rates, and expression of P-STAT3 (phosphorylated signal transduction and activators of transcription 3) and P-ERK (phosphorylated extracellular signal regulated protein kinase).

Results: Our data showed significant inhibition of growth, significantly increased S-phase arrest and apoptosis rates, and reduction of P-STAT3 and P-ERK1/2 expression levels.

Conclusions: We propose the mechanism may involve ARHI-induced phosphorylation of ERK1/2 and STAT3 protein kinases, thereby blocking proliferation signaling pathways, to induce HOC SKOV3 apoptosis.

*State Key Laboratory of Reproductive Medicine and †Department of Gynecology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing; and ‡Department of Gynecology and Obstetrics, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China.

Address correspondence and reprint requests to Yufei Shen, MD, State Key Laboratory of Reproductive Medicine, Department of Gynecology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, No. 123, Tianfei Lane, Mochou Rd, Nanjing, Jiangsu, 210029, People’s Republic of China. E-mail: syf09001397@163.com.

This project was supported by the Medical Science and Technology Development Foundation, Nanjing Department of Health of China (no. YKK10037).

The authors declare no conflicts of interest.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0.

Received July 9, 2013

Accepted January 7, 2014

© 2014 by the International Gynecologic Cancer Society and the European Society of Gynaecological Oncology.