S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines. Issue 4 (1st May 2014)

• Record Type: Journal Article
• Authors: Zhu, Qiaoying; Hu, Jianming; Meng, Huijuan; Shen, Yufei; Zhou, Jinhua; Zhu, Zhihong
• Is Part Of: International journal of gynecological cancer. Volume 24:Issue 4(2014)
• Page Start: 629
• Page End: 634
• Publication Date: 2014-05-01
• Subjects: Ovarian neoplasms -- ARHI -- SKOV3 -- STAT3 -- Autophagy -- ARHI-aplasia Ras homolog member I -- ERK-extracellular signal regulated protein kinase -- GAPDH-glyceraldehyde phosphate dehydrogenase -- GFP-green fluorescence protein -- IR-inhibitory rate -- OD-optical density -- P-STAT3-phosphorylated STAT3 -- STAT-signal transduction and activators of transcription; Generative organs, Female -- Cancer -- Periodicals; 616.99465
• DOI: 10.1097/IGC.0000000000000105
• Languages: English
• ISSNs: 1048-891X

Abstract

Abstract : 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.