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High glucose contributes to the proliferation and migration of non-small cell lung cancer cells via GAS5-TRIB3 axis.
Ding, Cheng-Zhi; Guo, Xu-Feng; Wang, Guo-Lei; Wang, Hong-Tao; Xu, Guang-Hui; Liu, Yuan-Yuan; Wu, Zhen-Jiang; Chen, Yu-Hang; Wang, Jiao; Wang, Wen-Guang.
Afiliação
  • Ding CZ; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Guo XF; Department of Thoracic Surgery, Shanghai Chest Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China, Shanghai, China.
  • Wang GL; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Wang HT; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Xu GH; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Liu YY; Department of Thoracic Surgery, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Wu ZJ; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Chen YH; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, China.
  • Wang J; Division of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China, Zhengzhou, China.
  • Wang WG; Department of Thoracic Oncology, Henan Provincial Chest Hospital, Zhengzhou, China, Zhengzhou, 450008, China xbtumor@163.com.
Biosci Rep ; 2018 Jan 24.
Article em En | MEDLINE | ID: mdl-29367413
ABSTRACT
Despite the growing number of studies exhibited an association of diabetes mellitus (DM) and lung cancer progression, the concrete mechanism of DM aggravating lung cancer has not been elucidated. This study was to investigate whether and how high glucose (HG) contribute to the proliferation and migration of non-small cell lung cancer (NSCLC) cells in vitro. In the present study, we confirmed that HG promoted the proliferation and migration of NSCLC cells, and also induced an anti-apoptosis effect on NSCLC cells. Moreover, HG inhibited the expression of GAS5 in NSCLC cells but elevated the protein level of TRIB3. GAS5 overexpression promoted the degradation of TRIB3 protein by ubiquitination and inhibited the HG induced-proliferation, anti-apoptosis and migration of NSCLC cells. Importantly, TRIB3 overexpression reversed the effects of GAS5 on the HG-treated NSCLC cells. Taken together, down-regulated GAS5 by HG significantly enhanced the proliferation, anti-apoptosis and migration in NSCLC cells through TRIB3, thus promoting the carcinogenesis of NSCLC.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Biosci Rep Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Biosci Rep Ano de publicação: 2018 Tipo de documento: Article