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An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
MicroRNA-92b acts as an oncogene by targeting PTEN/AKT in NSCLC
Jia-Hui Guo1, Hai-Yun Fang1, Jun-Mei Yang2
1Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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.
Insights
MicroRNA-92b acts as an oncogene in non-small cell lung cancer (NSCLC). Upregulated miR-92b promotes NSCLC growth and spread by targeting PTEN and activating AKT signaling.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are key regulators of cellular processes, acting as tumor suppressors or oncogenes.
- Dysregulation of miRNA is implicated in the development of non-small cell lung cancer (NSCLC).
Purpose of the Study:
- To investigate the role of miR-92b in NSCLC.
- To elucidate the molecular mechanism by which miR-92b influences NSCLC progression.
Main Methods:
- Quantitative real-time PCR to measure miR-92b expression in NSCLC tissues and cell lines.
- In vitro and in vivo assays to assess the effects of miR-92b knockdown and overexpression on NSCLC cell proliferation and migration.
- Western blotting and luciferase reporter assays to confirm the targeting of PTEN by miR-92b and its effect on the AKT pathway.
Main Results:
- miR-92b was significantly upregulated in human NSCLC tissues and cell lines.
- Knockdown of miR-92b inhibited NSCLC cell proliferation and migration in vitro and in vivo.
- Overexpression of miR-92b promoted an aggressive phenotype in NSCLC cells.
- miR-92b directly targets PTEN mRNA, leading to PTEN degradation and activation of the downstream AKT signaling pathway.
Conclusions:
- miR-92b functions as an oncogene in NSCLC by targeting the PTEN/AKT pathway.
- These findings highlight miR-92b as a potential therapeutic target for NSCLC treatment.
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