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Potential dual functional roles of the Y-linked RBMY in hepatocarcinogenesis
Tatsuo Kido1,2, Z Laura Tabatabai3, Xin Chen4,5
1Division of Cell and Developmental Genetics, Department of Medicine, San Francisco VA Health Care System, San Francisco, CA, USA.
Cancer Science
|May 31, 2020
Summary
The RNA-binding motif on the Y chromosome (RBMY) gene shows dual roles in hepatocellular carcinoma (HCC). While often linked to poor prognosis, RBMY overexpression unexpectedly inhibited HCC cell growth and tumor development in models.
Area of Science:
- Hepatocellular carcinoma (HCC) research
- Cancer genomics
- Molecular oncology
Background:
- Hepatocellular carcinoma (HCC) exhibits significant male biases in incidence and outcomes.
- The Y chromosome-linked RNA-binding motif on the Y chromosome (RBMY) gene is implicated in HCC oncogenesis.
- Previous studies suggest RBMY promotes liver cancer, but its precise role remains unclear.
Purpose of the Study:
- To investigate the role of RBMY in hepatocellular carcinoma (HCC).
- To determine the immediate effects of RBMY overexpression on liver cancer cells.
- To elucidate the impact of RBMY on HCC development in vivo.
Main Methods:
- Immunohistochemical analysis of HCC specimens.
- Data mining of The Cancer Genome Atlas (TCGA) database.
- Cell proliferation assays (HuH-7, HepG2) and transcriptome analysis.
- In vivo mouse liver cancer model with oncogene injection.
Main Results:
- High RBMY expression correlated with poor patient prognosis and survival.
- RBMY overexpression unexpectedly inhibited proliferation and induced cell death in HCC cell lines.
- RBMY downregulated key proliferative signaling pathways (RAS/RAF/MAP, PIP3/AKT).
- RBMY abolished HCC development in a mouse model.
Conclusions:
- RBMY exhibits context-dependent dual functions (tumor-suppressing and tumor-promoting) in HCC.
- Spatiotemporal expression and magnitude of RBMY influence its oncogenic role.
- RBMY may contribute to sexual dimorphisms observed in liver cancer.
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