PT  - JOURNAL ARTICLE
AU  - Zhu, Qiaoying
AU  - Hu, Jianming
AU  - Meng, Huijuan
AU  - Shen, Yufei
AU  - Zhou, Jinhua
AU  - Zhu, Zhihong
TI  - S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines
AID  - 10.1097/IGC.0000000000000105
DP  - 2014 May 01
TA  - International Journal of Gynecologic Cancer
PG  - 629--634
VI  - 24
IP  - 4
4099  - http://ijgc.bmj.com/content/24/4/629.short
4100  - http://ijgc.bmj.com/content/24/4/629.full
SO  - Int J Gynecol Cancer2014 May 01; 24
AB  - 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.