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lncRNA ADAMTS9-AS1/circFN1 Competitively Binds to miR-206 to Elevate the Expression of ACTB, Thus Inducing

Wei Feng1, Shuo Han2

  • 1Department of Ultrasound, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, China.

Oxidative Medicine and Cellular Longevity
|April 11, 2022
PubMed

Insights

This study reveals a novel regulatory network involving ADAMTS9-AS1, circFN1, miR-206, and ACTB in hypertrophic cardiomyopathy (HCM). This finding offers new insights into the molecular mechanisms underlying HCM development.

Area of Science:

  • Genetics
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Hypertrophic cardiomyopathy (HCM) is a genetic heart condition causing significant disability.
  • Understanding the molecular pathways involved in HCM is crucial for developing effective treatments.

Purpose of the Study:

  • To explore the potential roles of long noncoding RNA (lncRNA)-, circular RNA (circRNA)-, microRNA (miRNA)-, and messenger RNA (mRNA) networks in HCM.
  • To identify key regulatory elements and pathways implicated in HCM pathogenesis.

Main Methods:

  • Analysis of HCM-related microarray data from the GEO database to identify differentially expressed genes (DEGs).
  • Utilized GeneCards and CTD databases to retrieve HCM-related target genes and STRING database for network construction.
  • Predicted upstream lncRNAs, circRNAs, and miRNAs targeting ACTB using multiple bioinformatics tools.
  • Validated the expression of key molecules (ADAMTS9-AS1, circFN1, miR-206, ACTB) in patient samples and used cell lines for in vitro mechanistic studies.

Main Results:

  • Identified 15 candidate target genes related to HCM, with ACTB identified as a hub gene.
  • Established a regulatory network: ADAMTS9-AS1 and circFN1 act as upstream regulators of miR-206, which targets ACTB.
  • Observed decreased expression of ADAMTS9-AS1, circFN1, and ACTB, and increased expression of miR-206 in HCM patients.
  • In vitro experiments confirmed that ADAMTS9-AS1 and circFN1 competitively bind to miR-206, upregulating ACTB expression.

Conclusions:

  • The ADAMTS9-AS1/circFN1-miR-206-ACTB regulatory network is implicated in the occurrence of HCM.
  • This network provides a novel theoretical basis for understanding the molecular mechanisms of HCM.

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