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MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targeting MAPK1

Lei Chang1, Dongya Zhang1, Huirong Shi1

  • 1Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000 Henan, China.

Oncotarget
|November 16, 2017
PubMed

Insights

MicroRNA-143 (miR-143) is underexpressed in endometrial cancer (EC). Restoring miR-143 levels inhibits EC cell growth, migration, and invasion by targeting mitogen-activated protein kinase 1 (MAPK1).

Area of Science:

  • Gynecologic Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Endometrial cancer (EC) is a prevalent gynecologic malignancy with a high morbidity rate.
  • The underlying mechanisms of EC pathogenesis remain incompletely understood, hindering effective treatment strategies.
  • Identifying novel molecular targets is crucial for developing new therapeutic approaches for EC.

Purpose of the Study:

  • To investigate the regulatory relationship between miR-143 and mitogen-activated protein kinase 1 (MAPK1) in endometrial cancer.
  • To explore the functional impact of miR-143 on EC cell behavior, specifically proliferation, migration, and invasion, through its targeting of MAPK1.
  • To assess the potential of miR-143 as a therapeutic agent for endometrial cancer.

Main Methods:

  • Bioinformatic analysis to predict miR-143 target genes.
  • Quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot to assess miR-143 and MAPK1 expression in EC tissues and cells.
  • Transfection of miR-143 mimics and MAPK1 siRNA into EC cells (HEC-1B) to modulate gene expression.
  • In vitro assays including Cell Counting Kit-8, wound healing, flow cytometry, and Transwell assays to evaluate EC cell proliferation, migration, cell cycle, and invasion.

Main Results:

  • MiR-143 was significantly underexpressed in endometrial cancer tissues and cells compared to adjacent normal tissues.
  • Overexpression of miR-143 or knockdown of MAPK1 significantly inhibited EC cell proliferation, migration, and invasion, while inducing apoptosis.
  • MAPK1 was confirmed as a direct target gene of miR-143, and miR-143 overexpression led to decreased mRNA and protein levels of MAPK1 in EC cells.

Conclusions:

  • MiR-143 plays a tumor-suppressive role in endometrial cancer by inhibiting cell proliferation, migration, and invasion.
  • The tumor-suppressive effects of miR-143 are mediated, at least in part, by the direct suppression of MAPK1 expression.
  • MiR-143 represents a potential novel therapeutic target for the clinical management of endometrial cancer.
Keywords:
MAPK1endometrial cancermiR-143migrationproliferation

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