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

Junji Kurashige, Hidenobu Kamohara, Masayuki Watanabe, Yukiharu Hiyoshi, Masaaki Iwatsuki, Youhei Tanaka, Koichi Kinoshita, Seiya Saito, Yoshifumi Baba, Hideo Baba

Research output: Contribution to journalArticle

137 Citations (Scopus)

Abstract

Background: The microRNA-200 (miR-200) family has been reported to induce epithelial differentiation and suppress epithelial-mesenchymal transition (EMT) by inhibiting translation of zinc finger E-box-binding homeobox (ZEB) 1 and 2 mRNAs in several types of cancers. This study aimed to clarify the role of miR-200b in regulating EMT and promoting cellular proliferation, invasion, and migration in gastric cancer. Methods: The relationships among the expression levels of miR-200b, ZEB1 and ZEB2, and E-cadherin mRNAs were analyzed by quantitative real-time reverse transcription-polymerase chain reaction in frozen tissue samples from 40 gastric cancer patients who underwent gastrectomy from 2008 to 2010. The effects of miR-200b on EMT in gastric cancer cells in vitro were also analyzed. Results: Diffuse histologic type, depth of tumor, tumor size, lymph node metastasis, and lymphatic invasion were significantly higher in the low-miR-200b expression group compared with the high expression group. There was a strong correlation between the levels of miR-200b, and ZEB2 and E-cadherin mRNAs in gastric cancer patients. Upregulation of miR-200b in gastric cancer cells changed the cell morphology from fibroblast- to epithelial-like, associated with localization of E-cadherin to the plasma membrane. ZEB2 mRNA levels fell, while E-cadherin expression levels increased in gastric cells overexpressing miR-200b, associated with significantly reduced cellular proliferation, and inhibition of cellular migration and invasion. Conclusions: miR-200b regulates ZEB2 expression and thus controls metastasis in gastric cancer.

Original languageEnglish
JournalAnnals of Surgical Oncology
Volume19
Issue numberSUPPL. 3
DOIs
Publication statusPublished - Jul 1 2012

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MicroRNAs
Stomach Neoplasms
Cell Movement
Stomach
Cell Proliferation
Cadherins
Carcinoma
Epithelial-Mesenchymal Transition
Messenger RNA
Lymphatic Metastasis
Neoplasms
Gastrectomy
Reverse Transcription
Up-Regulation
Fibroblasts
Lymph Nodes
Cell Membrane
Neoplasm Metastasis
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Surgery
  • Oncology

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MicroRNA-200b regulates cell proliferation, invasion, and migration by directly targeting ZEB2 in gastric carcinoma. / Kurashige, Junji; Kamohara, Hidenobu; Watanabe, Masayuki; Hiyoshi, Yukiharu; Iwatsuki, Masaaki; Tanaka, Youhei; Kinoshita, Koichi; Saito, Seiya; Baba, Yoshifumi; Baba, Hideo.

In: Annals of Surgical Oncology, Vol. 19, No. SUPPL. 3, 01.07.2012.

Research output: Contribution to journalArticle

Kurashige, J, Kamohara, H, Watanabe, M, Hiyoshi, Y, Iwatsuki, M, Tanaka, Y, Kinoshita, K, Saito, S, Baba, Y & Baba, H 2012, 'MicroRNA-200b regulates cell proliferation, invasion, and migration by directly targeting ZEB2 in gastric carcinoma', Annals of Surgical Oncology, vol. 19, no. SUPPL. 3. https://doi.org/10.1245/s10434-012-2217-6
Kurashige, Junji ; Kamohara, Hidenobu ; Watanabe, Masayuki ; Hiyoshi, Yukiharu ; Iwatsuki, Masaaki ; Tanaka, Youhei ; Kinoshita, Koichi ; Saito, Seiya ; Baba, Yoshifumi ; Baba, Hideo. / MicroRNA-200b regulates cell proliferation, invasion, and migration by directly targeting ZEB2 in gastric carcinoma. In: Annals of Surgical Oncology. 2012 ; Vol. 19, No. SUPPL. 3.
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AU - Kurashige, Junji

AU - Kamohara, Hidenobu

AU - Watanabe, Masayuki

AU - Hiyoshi, Yukiharu

AU - Iwatsuki, Masaaki

AU - Tanaka, Youhei

AU - Kinoshita, Koichi

AU - Saito, Seiya

AU - Baba, Yoshifumi

AU - Baba, Hideo

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N2 - Background: The microRNA-200 (miR-200) family has been reported to induce epithelial differentiation and suppress epithelial-mesenchymal transition (EMT) by inhibiting translation of zinc finger E-box-binding homeobox (ZEB) 1 and 2 mRNAs in several types of cancers. This study aimed to clarify the role of miR-200b in regulating EMT and promoting cellular proliferation, invasion, and migration in gastric cancer. Methods: The relationships among the expression levels of miR-200b, ZEB1 and ZEB2, and E-cadherin mRNAs were analyzed by quantitative real-time reverse transcription-polymerase chain reaction in frozen tissue samples from 40 gastric cancer patients who underwent gastrectomy from 2008 to 2010. The effects of miR-200b on EMT in gastric cancer cells in vitro were also analyzed. Results: Diffuse histologic type, depth of tumor, tumor size, lymph node metastasis, and lymphatic invasion were significantly higher in the low-miR-200b expression group compared with the high expression group. There was a strong correlation between the levels of miR-200b, and ZEB2 and E-cadherin mRNAs in gastric cancer patients. Upregulation of miR-200b in gastric cancer cells changed the cell morphology from fibroblast- to epithelial-like, associated with localization of E-cadherin to the plasma membrane. ZEB2 mRNA levels fell, while E-cadherin expression levels increased in gastric cells overexpressing miR-200b, associated with significantly reduced cellular proliferation, and inhibition of cellular migration and invasion. Conclusions: miR-200b regulates ZEB2 expression and thus controls metastasis in gastric cancer.

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