Long Noncoding RNA TFAP2A-AS1 Suppressed Hepatitis B Virus Replication by Modulating miR-933/HDAC11

Area of Science:

• Molecular Biology
• Hepatology
• Oncology

Background:

• Long noncoding RNAs (lncRNAs) are implicated in various cancers, including hepatocellular carcinoma (HCC).
• Hepatitis B virus (HBV) infection is a major cause of HCC, and its molecular mechanisms are not fully understood.
• The role of specific lncRNAs, such as TFAP2A-AS1, in HBV-associated HCC requires further investigation.

Purpose of the Study:

• To investigate the role of lncRNA TFAP2A-AS1 in hepatocellular carcinoma (HCC) with hepatitis B virus (HBV) infection.
• To elucidate the regulatory mechanism of TFAP2A-AS1 in HBV replication and HCC progression.

Main Methods:

• Quantitative reverse transcription PCR (qRT-PCR) to assess TFAP2A-AS1 and miR-933 levels.
• Luciferase reporter gene assays to determine interactions between TFAP2A-AS1, miR-933, and HDAC11.
• Cell proliferation assays (CCK-8) and HBV DNA replication detection (RT-qPCR).

Main Results:

• TFAP2A-AS1 was downregulated, while miR-933 was upregulated in HCC cell lines and HBV-infected HCC samples.
• TFAP2A-AS1 functioned as a molecular sponge for miR-933, and HDAC11 was a direct target of miR-933.
• Overexpression of TFAP2A-AS1 suppressed cell growth, HBV DNA replication, HBeAg, and HBsAg expression, whereas miR-933 promoted these processes.

Conclusions:

• TFAP2A-AS1 plays a critical role in regulating HBeAg and HBsAg expression and HBV replication.
• TFAP2A-AS1 may serve as a potential therapeutic target for HBV infection-related HCC.