MiR-181c affects estrogen-dependent endometrial carcinoma cell growth by targeting PTEN

Lili Zhuang1, Hongmei Qu2, Jianxiang Cong1

  • 1Department of Center for Reproductive Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, China.

Endocrine Journal
|April 12, 2019
PubMed

Insights

MicroRNAs (miRNAs) regulate endometrial cancer cell growth. miR-181c targets PTEN, promoting apoptosis in estrogen-dependent cancer cells, suggesting it as a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression by binding to mRNA targets.
  • Endometrial carcinoma is an estrogen-dependent cancer with complex regulatory mechanisms.
  • Understanding miRNA roles is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the role and mechanism of miR-181c in the apoptosis of RL95-2 human endometrial carcinoma cells.
  • To determine if miR-181c affects estrogen-induced cell activity and apoptosis.
  • To identify the molecular targets of miR-181c in this cellular context.

Main Methods:

  • Cell viability assessed using cell counting Kit-8 (CCK-8) assay.
  • Apoptosis detected by flow cytometry (FCM).
  • Gene and protein expression analyzed via qRT-PCR and Western blot; miRNA-target interaction confirmed by luciferase reporter assay.

Main Results:

  • Estrogen (E2) increased RL95-2 cell activity.
  • miR-181c inhibition suppressed cell viability and enhanced apoptosis in E2-treated cells.
  • miR-181c directly targets PTEN, upregulating its expression and promoting apoptosis via Bax/Bcl-2, AKT, p53, and Cyclin D modulation.

Conclusions:

  • miR-181c influences estrogen-dependent endometrial carcinoma cell growth by targeting PTEN.
  • miR-181c promotes apoptosis in E2-induced RL95-2 cells.
  • miR-181c represents a potential therapeutic target for endometrial carcinoma treatment.

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