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MicroRNA-92b acts as an oncogene by targeting PTEN/AKT in NSCLC.
Guo, Jia-Hui; Fang, Hai-Yun; Yang, Jun-Mei; Liu, Shan-Ling; Yao, Qiang-Hua; Fan, Yi-Juan; Zhao, Mei; Liu, Feng; Zhang, Quan-Wu; Gao, Feng-Hou.
Afiliação
  • Guo JH; Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Fang HY; Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Yang JM; Department of Clinical Laboratory, Children's Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
  • Liu SL; Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Yao QH; Department of Pediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Fan YJ; Department of Pathology, Huashan-Baoshan Hospital, Shanghai, China.
  • Zhao M; Department of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China.
  • Liu F; Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Zhang QW; Department of Pathology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
  • Gao FH; Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Cell Biochem Funct ; 38(8): 1100-1110, 2020 Dec.
Article em En | MEDLINE | ID: mdl-32627866
ABSTRACT
MicroRNAs can act as tumour suppressors or oncogenes by regulating cellular differentiation, proliferation and apoptosis, and the dysregulation of miRNA is involved in the occurrence and development of NSCLC. Here, we provided evidence that miR-92b as an oncogene in NSCLC by targeting PTEN/AKT. We found that miR-92b was up-regulated in human NSCLC tissues and cell lines. MiR-92b knockdown suppressed the NSCLC cells proliferation and migration in both in vivo and in vitro models. Conversely, miR-92b overexpression induced an aggressive phenotype. Moreover, miR-92b-mediated regulation of NSCLC cell proliferation and migration depended on binding to PTEN mRNA, which then led to the degradation of PTEN and activation of the downstream AKT signalling pathway. Overall, this study revealed the oncogenic roles of miR-92b in NSCLC by targeting PTEN/AKT, and provided novel insights for future treatments of NSCLC patients. SIGNIFICANCE OF THE STUDY MiR-92b was up-regulated in human NSCLC tissues and cell lines. Our study demonstrated that miR-92b as an oncogene in NSCLC by targeting PTEN/AKT in both in vivo and in vitro models and provided novel insights for future treatments of NSCLC patients.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Oncogenes / RNA Neoplásico / Carcinoma Pulmonar de Células não Pequenas / MicroRNAs / PTEN Fosfo-Hidrolase / Proteínas Proto-Oncogênicas c-akt / Neoplasias Pulmonares Limite: Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Oncogenes / RNA Neoplásico / Carcinoma Pulmonar de Células não Pequenas / MicroRNAs / PTEN Fosfo-Hidrolase / Proteínas Proto-Oncogênicas c-akt / Neoplasias Pulmonares Limite: Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article