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MicroRNA-200b regulates cell proliferation, invasion, and migration by directly targeting ZEB2 in gastric carcinoma

Junji Kurashige1, Hidenobu Kamohara, Masayuki Watanabe

  • 1Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Annals of Surgical Oncology
|February 8, 2012
PubMed
Abstract

Insights

MicroRNA-200b (miR-200b) suppresses metastasis in gastric cancer by regulating ZEB2 expression. Upregulating miR-200b inhibits cell proliferation, migration, and invasion, promoting epithelial differentiation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • The microRNA-200 (miR-200) family inhibits epithelial-mesenchymal transition (EMT) by targeting zinc finger E-box-binding homeobox (ZEB) 1 and 2.
  • EMT is implicated in cancer progression, including in gastric cancer.

Purpose of the Study:

  • To investigate the role of miR-200b in regulating EMT in gastric cancer.
  • To determine the impact of miR-200b on gastric cancer cell proliferation, invasion, and migration.

Main Methods:

  • Quantitative real-time reverse transcription-polymerase chain reaction was used to analyze miR-200b, ZEB1, ZEB2, and E-cadherin mRNA levels in 40 gastric cancer patient samples.
  • In vitro experiments assessed the effects of miR-200b on gastric cancer cell EMT.

Main Results:

  • Low miR-200b expression correlated with higher rates of diffuse histologic type, deeper tumor invasion, larger tumor size, lymph node metastasis, and lymphatic invasion.
  • miR-200b levels were strongly correlated with ZEB2 and E-cadherin mRNA.
  • Overexpression of miR-200b in gastric cancer cells induced an epithelial phenotype, reduced ZEB2 expression, increased E-cadherin, and inhibited proliferation, migration, and invasion.

Conclusions:

  • miR-200b plays a critical role in controlling metastasis in gastric cancer.
  • miR-200b regulates ZEB2 expression, impacting EMT and cancer progression.

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