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Title:
MicroRNA-200b Regulates Cell Proliferation, Invasion, and Migration by Directly Targeting ZEB2 in Gastric Carcinoma | Annals of Surgical Oncology
Description:
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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Keywords {🔍}
article, cancer, google, scholar, pubmed, cas, gastric, cell, zeb, expression, cells, ecadherin, invasion, phd, mirb, microrna, epithelial, epithelialmesenchymal, metastasis, targeting, carcinoma, tumor, inhibits, nat, research, regulates, proliferation, migration, family, transition, access, biol, res, privacy, cookies, content, baba, tumour, lee, publish, search, kamohara, emt, levels, upregulation, progression, breast, sip, mol, pathol,
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mir-200c inhibits tgf-β-induced-emt suppress epithelial–mesenchymal transition month download article/chapter mir-200b mrna expression mir-10b inhibits metastasis e-cadherin gene expression intestinal-type gastric carcinogenesis microrna-200c mitigates invasiveness increased cell-cell adhesion myc/mycn-activated microrna mir-200a-mediated downregulation polycomb-mediated repression required epithelial cell–cell junctions microtubule-targeting chemotherapeutic agents e-cadherin repressors zeb1 paclitaxel-based treatment response pre-mir-200b showed hideo baba md surgical oncology aims sip1/zeb2 induces emt related subjects gastric cancer cells epithelial–mesenchymal transitions high expression group mirna expression profiling repressing stemness-inhibiting micrornas regulates epithelial plasticity mir-205 regulate epithelial full article pdf gastric cancer patients cancer stem cells breast cancer cells mesenchymal transition regulates e-cadherin human breast cancer gastric cancer prognosis privacy choices/manage cookies hsa-mir-200c increases cell proliferation mir-200 family determines transcription factor zeb1 directly targeting zeb2 yukiharu hiyoshi md masaaki iwatsuki md normal stem cells epithelial tumour cells transcription factor snail clin cancer res human ovarian cancer ovarian cancer patients
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headline:MicroRNA-200b Regulates Cell Proliferation, Invasion, and Migration by Directly Targeting ZEB2 in Gastric Carcinoma
description: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. 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. 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. miR-200b regulates ZEB2 expression and thus controls metastasis in gastric cancer.
datePublished:2012-02-04T00:00:00Z
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Gastric Cancer
Gastric Cancer Cell
Gastric Cancer Patient
ZEB2 Expression
ZEB2 mRNA
Surgical Oncology
Oncology
Surgery
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headline:MicroRNA-200b Regulates Cell Proliferation, Invasion, and Migration by Directly Targeting ZEB2 in Gastric Carcinoma
description: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. 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. 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. miR-200b regulates ZEB2 expression and thus controls metastasis in gastric cancer.
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Gastric Cancer Cell
Gastric Cancer Patient
ZEB2 Expression
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Surgical Oncology
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Surgery
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