Expression Analysis and Correlation of miR-193b-5p with CLTC and AP2M1 in NASH-Associated Hepatocellular Carcinoma

Document Type : Original Article

Authors
1 Department of Biology, Jahrom Branch, Islamic Azad University, Jahrom, Iran
2 Department of Biology, ShK.C., Islamic Azad University, Shahrekord, Iran.
3 Department of Biology, Arsanjan branch, Islamic Azad University, Arsanjan, Iran
4 Department of Biology, Jahrom Branch, Islamic Azad University,Jahrom, Iran
Abstract
Background: It is predicted that over 30% of adults will be affected by non-alcoholic fatty liver disease (NAFLD), with approximately 20% of these cases progressing to non-alcoholic steatohepatitis (NASH). Due to these trends, cases of hepatocellular carcinoma (HCC) and NASH-related liver transplants are expected to double by 2030. The development of targeted therapies requires an understanding of the genetic and regulatory mechanisms involving non-coding RNAs (ncRNAs) in NASH.

Methods: We investigated the regulatory interaction between CLTC, AP2M1, and miR-193b-5p through comprehensive bioinformatics (in silico) analyses and then validated it experimentally using molecular methods, including qRT-PCR.

Results: qRT-PCR data demonstrated that miR-193 expression was significantly decreased in the liver tissue of HCC patients compared to the control group. Furthermore, correlation analysis revealed a negative correlation between miR-193 and CLTC and AP2M1 genes, indicating its potential regulatory role in pathways associated with NASH progression and liver carcinogenesis.

Conclusion: miR-193 was identified as a miRNA with consistently reduced expression in liver cancer (LIHC), suggesting its potential regulatory role in the progression of liver diseases. Integrated bioinformatics analyses showed that CLTC and AP2M1 genes, which are inversely correlated with miR-193, are enriched in pathways related to lipid metabolism, vesicle-mediated transport, endocytosis, and survival-related signaling pathways—pathways closely associated with NASH progression and liver carcinogenesis.
Keywords

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