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: email@example.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.
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Received July 9, 2013
Accepted January 7, 2014