MiRNA- 1293 Promotes Hepatocellular Carcinoma Cell Proliferation and Invasion by METTL3-Mediated m6 A Modification of Pri-miRNA- 1293
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View abstract on PubMed
Summary
This summary is machine-generated.MicroRNA-1293 (miR-1293) promotes hepatocellular carcinoma (HCC) progression by enhancing cell viability and invasion. METTL3-mediated m6A methylation regulates miR-1293, offering potential new therapeutic strategies for HCC.
Area Of Science
- Oncology
- Molecular Biology
- Epigenetics
Background
- Hepatocellular carcinoma (HCC) is an aggressive digestive system malignancy.
- MicroRNAs (miRNAs) and N6-methyladenine (m6A) modification are implicated in HCC progression.
- The specific roles of miR-1293 and its regulatory mechanisms in HCC require further elucidation.
Purpose Of The Study
- To investigate the role of miR-1293 in hepatocellular carcinoma (HCC) progression.
- To elucidate the underlying molecular mechanism involving m6A modification and METTL3.
Main Methods
- Quantitative real-time PCR, methylated RNA immunoprecipitation (MeRIP), and RNA immunoprecipitation (RIP).
- Cell counting kit-8 and Transwell assays to assess cellular biological behaviors.
- Xenograft tumor experiments in vivo.
Main Results
- miR-1293 was significantly upregulated in HCC tissues and cell lines.
- Overexpression of miR-1293 enhanced HCC cell viability, invasion, and migration.
- METTL3 accelerated pri-miR-1293 processing and maturation in an m6A-dependent manner.
- miR-1293 promoted tumor growth in vivo.
Conclusions
- miR-1293 plays a crucial role in promoting HCC progression.
- The METTL3-mediated m6A methylation pathway regulates miR-1293 levels and function in HCC.
- Targeting the miR-1293/METTL3 axis presents a potential therapeutic strategy for HCC.
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