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MicroRNA-153 regulated AKT1 expression and suppressed cell proliferation of epithelial ovarian cancer cells

Weizhen Li1, Mengjie Wang2,3, Bi Meng2,3

  • 1Department of Clinical Laboratory, The Taixing People's Hospital Taixing, Jiangsu, China.

International Journal of Clinical and Experimental Pathology
|January 23, 2020
PubMed

Insights

MicroRNA-153 (miR-153) is downregulated in epithelial ovarian cancer (EOC), suppressing tumor growth and migration by targeting AKT1. This suggests miR-153 has potential as a therapeutic target for ovarian cancer.

Area of Science:

  • Molecular Oncology
  • Biochemistry
  • Genetics

Background:

  • Epithelial ovarian cancer (EOC) is a leading cause of cancer-related deaths in women globally, with rising incidence in China.
  • Dysregulation of microRNAs (miRNAs), such as miR-153, is implicated in various human cancers, including EOC.
  • Understanding the role of miR-153 and its targets in EOC is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the functional roles of miR-153 and its target gene AKT1 in regulating the growth and migration of epithelial ovarian cancer cells.
  • To explore the potential of miR-153 as a prognostic or therapeutic agent for ovarian cancer patients.

Main Methods:

  • Quantitative real-time RT-PCR was used to measure miR-153 expression levels in EOC tissues and normal tissues.
  • Cell proliferation was assessed using CCK-8 assays, and cell cycle analysis was performed via flow cytometry.
  • Dual-luciferase reporter assays confirmed AKT1 as a direct target of miR-153.

Main Results:

  • miR-153 expression was significantly lower in EOC tissues compared to matched normal tissues.
  • Overexpression of miR-153 induced G0/G1 cell cycle arrest and suppressed proliferation and migration in EOC cells.
  • AKT1 was identified as a direct target of miR-153, and its overexpression reversed the inhibitory effects of miR-153.

Conclusions:

  • miR-153 inhibits EOC cell proliferation and migration by directly targeting AKT1.
  • Restored miR-153 levels can impede ovarian cancer progression.
  • miR-153 holds promise as a potential biomarker and therapeutic target for epithelial ovarian cancer management.
Keywords:
AKT1Epithelial ovarian cancermicroRNA-153

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