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Upregulation of miR-200b Inhibits Hepatocellular Carcinoma Cell Proliferation and Migration by Targeting HMGB3 Protein.
Wang, Long-Kun; Xie, Xi-Na; Song, Xu-Hong; Su, Ting; Chang, Xiao-Lan; Xu, Man; Liang, Bin; Huang, Dong-Yang.
Afiliación
  • Wang LK; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Xie XN; 2 Institute of Translational Medicine, Shenzhen Second People Hospital, The First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen, China.
  • Song XH; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Su T; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Chang XL; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Xu M; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Liang B; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
  • Huang DY; 1 Department of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Shantou University Medical College, Shantou, China.
Technol Cancer Res Treat ; 17: 1533033818806475, 2018 01 01.
Article en En | MEDLINE | ID: mdl-30343649
HMGB3 belongs to the high-mobility group box subfamily and has been found to be overexpressed in gastric cancer. However, the expression and the role of HMGB3 in human hepatocellular carcinoma remain unknown. Here, we report that HMGB3, which is suppressed by miR-200b, contributes to cell proliferation and migration in human hepatocellular carcinoma. After analyzing The Cancer Genome Atlas data of 371 patients with hepatocellular carcinoma, we identified HMGB3 to be upregulated in human hepatocellular carcinoma tissue. Knockdown of HMGB3 in the hepatocellular carcinoma cell line suppressed cell proliferation and migration. TargetScan analysis showed miR-200b to be a possible regulator for HMGB3. Subsequent luciferase assays indicated that HMGB3 was a direct target of miR-200b. In addition, upregulation of miR-200b inhibited hepatocellular carcinoma cell growth and migration. HMGB3 overexpression or miR-200b downregulation was associated with poor prognosis. Our findings suggest HMGB3 may serve as an important oncoprotein whose expression is negatively regulated by miR-200b in hepatocellular carcinoma.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Regulación Neoplásica de la Expresión Génica / Carcinoma Hepatocelular / Proteína HMGB3 / MicroARNs / Interferencia de ARN / Neoplasias Hepáticas Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Technol Cancer Res Treat Asunto de la revista: NEOPLASIAS / TERAPEUTICA Año: 2018 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Regulación Neoplásica de la Expresión Génica / Carcinoma Hepatocelular / Proteína HMGB3 / MicroARNs / Interferencia de ARN / Neoplasias Hepáticas Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Technol Cancer Res Treat Asunto de la revista: NEOPLASIAS / TERAPEUTICA Año: 2018 Tipo del documento: Article País de afiliación: China