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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
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circHIPK3 Acts as Competing Endogenous RNA and Promotes Non-Small-Cell Lung Cancer Progression through the
Weijun Hong1, Yajuan Zhang1, Jingyi Ding1
1Department of Respiratory Medicine, Minhang Hospital, Fudan University, China.
Biomed Research International
|October 5, 2020
Summary
Circular RNA HIPK3 (circHIPK3) promotes non-small-cell lung cancer (NSCLC) progression by interacting with miR-107 and brain-derived neurotrophic factor (BDNF). Targeting this circHIPK3/miR-107/BDNF axis may offer new treatments for NSCLC.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Circular RNAs (circRNAs) play significant roles in human diseases, especially cancers.
- circRNA HIPK3 (circHIPK3) is implicated in non-small-cell lung cancer (NSCLC) oncogenesis, but its regulatory mechanism remains unclear.
Purpose of the Study:
- To investigate the role of circHIPK3 in NSCLC progression.
- To elucidate the regulatory pathway involving circHIPK3, miR-107, and brain-derived neurotrophic factor (BDNF) in NSCLC.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) to assess circHIPK3 expression in NSCLC.
- circHIPK3 knockdown and miR-107/BDNF overexpression experiments to evaluate functional impacts.
- Dual-luciferase reporter assays to confirm interactions between circHIPK3, miR-107, and BDNF.
Main Results:
- circHIPK3 expression was significantly upregulated in NSCLC cells.
- circHIPK3 knockdown suppressed NSCLC cell migration and proliferation by upregulating miR-107.
- circHIPK3 acts as a miR-107 sponge, promoting BDNF-mediated proliferation; miR-107 directly targets BDNF.
Conclusions:
- circHIPK3 promotes NSCLC progression via the circHIPK3/miR-107/BDNF axis.
- This pathway presents potential therapeutic targets and biomarkers for NSCLC treatment.
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