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Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor LATS Biosensor
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RP11-40C6.2 Inactivates Hippo Signaling by Attenuating YAP1 Ubiquitylation in Hepatitis B Virus-associated
Han Zhuo1, Chen Wu1, Junwei Tang2
1Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
Journal of Clinical and Translational Hepatology
|January 16, 2023
Summary
Hepatitis B virus (HBV) infection-associated long noncoding RNA RP11-40C6.2 promotes hepatocellular carcinoma (HCC) by activating the Hippo signaling pathway. This lncRNA stabilizes YAP1, driving tumor growth in HBV-related liver cancer.
Area of Science:
- Oncology
- Hepatology
- Molecular Biology
Background:
- Chronic hepatitis B virus (HBV) infection is a primary driver of hepatocellular carcinoma (HCC).
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
- Understanding HBV-associated lncRNAs is crucial for targeting HCC pathogenesis.
Purpose of the Study:
- To identify and characterize oncogenic HBV infection-associated lncRNAs in HCC.
- To elucidate the molecular mechanisms by which these lncRNAs contribute to HCC.
- To investigate the role of RP11-40C6.2 in HBV-related liver cancer.
Main Methods:
- Bioinformatic analysis of TCGA-Liver Hepatocellular Carcinoma database to screen for HBV-related lncRNAs.
- Expression analysis in clinical HCC samples and correlation with clinical characteristics.
- In vitro and in vivo studies to determine oncogenic functions and molecular pathways.
Main Results:
- RP11-40C6.2, an HBV-related lncRNA, was identified and found to be overexpressed in HCC with HBV infection.
- RP11-40C6.2 expression positively correlated with HBV-X protein (HBx).
- RP11-40C6.2 activates the Hippo signaling pathway by stabilizing YAP1, promoting HCC progression.
Conclusions:
- RP11-40C6.2 is an oncogenic lncRNA associated with HBV infection in HCC.
- RP11-40C6.2 exerts its oncogenic effects through the Hippo signaling pathway.
- Targeting RP11-40C6.2 may offer a therapeutic strategy for HBV-related HCC.
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