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MiR-26a enhances invasive capacity by suppressing GSK3ß in human lung cancer cells.
Lin, Gaoyang; Liu, Boning; Meng, Zhaowei; Liu, Yunde; Li, Xuebing; Wu, Xiang; Zhou, Qinghua; Xu, Ke.
Afiliação
  • Lin G; Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Liu B; Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Meng Z; Department of Nuclear Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Liu Y; School of Laboratory Medicine, Tianjin Medical University, Tianjin 300052, China.
  • Li X; Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Wu X; Core Facility Center, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Zhou Q; Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
  • Xu K; Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China. Electronic address: ke_xu@hotmail.com.
Exp Cell Res ; 352(2): 364-374, 2017 03 15.
Article em En | MEDLINE | ID: mdl-28237093
Lung cancer is the common cause of death from cancer, and most lung cancer patients die of metastasis. MicroRNAs (miRNAs) function as either oncogenes or tumor suppressors, playing crucial role not only in tumorigenesis, but also in tumor invasion and metastasis. There are several studies showed that miR-26a is involved in carcinogenesis, however, its role in tumor metastasis need to be elucidated. In this study, we showed that ectopic expression of miR-26a enhanced migration and invasion of lung cancer cells. Glycogen synthase kinase-3ß (GSK3ß) was identified as a direct target of miR-26a. GSK3ß expression negatively correlated with miR-26a expression in lung cancer tissues. Silencing of GSK3ß achieved similar effect as miR-26a over-expression; over-expression of GSK3ß reversed the enhanced effect of miR-26a on lung cancer cell migration and invasion. Further study indicated that miR-26a increased ß-catenin expression and nuclear translocation. C-myc and cyclin D1, the downstream genes of ß-catenin, were also up-regulated by miR-26a. Furthermore, xenograft study showed that miR-26a promoted lung cancer cell growth in vivo, and suppressed GSK3ß expression. Collectively, our results demonstrated that miR-26a enhanced metastatic potential of lung cancer cells via activation of ß-catenin pathway by targeting GSK3ß, suggesting the potential applicability of miR-26a as a target for cancer treatment.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: MicroRNAs / Glicogênio Sintase Quinase 3 beta / Neoplasias Pulmonares Limite: Animals / Female / Humans Idioma: En Revista: Exp Cell Res Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: MicroRNAs / Glicogênio Sintase Quinase 3 beta / Neoplasias Pulmonares Limite: Animals / Female / Humans Idioma: En Revista: Exp Cell Res Ano de publicação: 2017 Tipo de documento: Article