Activation of lncRNA DANCR by H3K27 acetylation regulates proliferation of colorectal cancer cells
View abstract on PubMed
Summary
This summary is machine-generated.The long noncoding RNA DANCR promotes colorectal cancer (CRC) progression by increasing cell proliferation and is upregulated by H3K27 acetylation. DANCR may serve as a therapeutic target for CRC.
Area Of Science
- Oncology
- Molecular Biology
- Epigenetics
Background
- Long noncoding RNA DANCR acts as an oncogene in various cancers.
- The specific molecular mechanisms of DANCR in colorectal cancer (CRC) remain largely unexplored.
Purpose Of The Study
- To investigate the function and molecular mechanism of DANCR in CRC progression.
- To identify potential therapeutic targets for CRC based on DANCR's role.
Main Methods
- Quantitative real-time PCR to assess DANCR expression.
- Cell proliferation assays and Western blotting to evaluate DANCR's functional impact.
- Bioinformatic analysis, luciferase reporter assays, and subcellular fractionation to determine molecular interactions.
- Chromatin immunoprecipitation assays to investigate epigenetic regulation.
Main Results
- DANCR was found to be overexpressed in CRC tissues and cell lines.
- Knockdown of DANCR inhibited CRC cell proliferation by downregulating cyclin D1 and CDK4.
- DANCR directly binds to miR-508-5p, functioning as a competing endogenous RNA (ceRNA) to regulate ATF1 expression.
- Upregulation of DANCR was linked to H3K27 acetylation at its promoter region.
Conclusions
- Activation of lncRNA DANCR via H3K27 acetylation plays a significant oncogenic role in CRC progression.
- DANCR's mechanism involves regulating cell proliferation and gene expression through the miR-508-5p/ATF1 axis.
- DANCR represents a potential therapeutic target for colorectal cancer treatment.
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