You are here

  • Home
  • Archive
  • Volume 24, Issue 4
  • S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines

Article Text

Article menu
Download PDFPDF
Basic Science
S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines
  1. Qiaoying Zhu, MD*,†,
  2. Jianming Hu, MD‡,
  3. Huijuan Meng, MD‡,
  4. Yufei Shen, MD*,†,
  5. Jinhua Zhou, MD‡ and
  6. Zhihong Zhu, MD†
  1. *State Key Laboratory of Reproductive Medicine and
  2. †Department of Gynecology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing; and
  3. ‡Department of Gynecology and Obstetrics, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China.
  1. 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{at}163.com.

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.

  • 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

https://doi.org/10.1097/IGC.0000000000000105

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Footnotes

    • 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.