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Thesis
Interplay of hepatitis B virus and lncRNA FAM99A expression and interacting proteins in liver cancer cell lines
Master of Science (M.S.), Drexel University
May 2024
DOI:
https://doi.org/10.17918/00010467
Abstract
Hepatocellular carcinoma (HCC), a primary liver malignancy, is responsible for approximately 90% of liver cancers and is a leading cause of cancer-related deaths globally. Despite its prevalence and impact, the molecular mechanisms driving the development, maintenance, and progression of HCC remain poorly understood, resulting in limited treatment options and a poor prognosis that is dependent on the stage of the tumor. Recent research has highlighted the important role of long non-coding RNAs (lncRNAs), which are RNA transcripts longer than 200 nucleotides that have no protein-coding potential, in regulating cellular signaling pathways and disease progression. To investigate the potential involvement of lncRNAs in HCC, we performed a comparative analysis of HCC tissue and adjacent nontumor tissue transcriptome data from The Cancer Genome Atlas (TCGA). We identified FAM99A, a liver-specific lncRNA, as significantly downregulated in HCC. Moreover, Kaplan-Meier analysis revealed a correlation between low FAM99A expression and poor overall survival in HCC patients. To further explore the functional role of FAM99A in HCC, we assessed its expression levels in liver cancer cell lines (HepG2, Huh7, and Hep3B) and primary human hepatocytes using quantitative PCR analysis. The results confirmed significantly lower FAM99A expression in liver cancer cell lines compared to primary human hepatocytes. Additionally, TREX and mass spectrometry assays were conducted to identify FAM99A's interacting partners. Accumulating evidence suggests that certain lncRNAs are dysregulated in HBV-related HCC and may influence the HBV lifecycle. Characterizing the functions of these lncRNAs can provide a more comprehensive understanding of HBV replication and oncogenesis. Intriguingly, we observed a significant decrease in FAM99A expression in cells transfected with a replication-competent cDNA of HBV, indicating that HBV downregulates FAM99A expression. In conclusion, our findings suggest that FAM99A is a potential tumor suppressor in HCC, and its downregulation by HBV may contribute to the development of HBV-associated HCC. These insights underscore the importance of further research into the role of FAM99A in HCC and its potential as a therapeutic target or prognostic marker.
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Details
- Title
- Interplay of hepatitis B virus and lncRNA FAM99A expression and interacting proteins in liver cancer cell lines
- Creators
- Ranjit Kaur
- Contributors
- Michael Bouchard (Advisor)
- Awarding Institution
- Drexel University
- Degree Awarded
- Master of Science (M.S.)
- Publisher
- Drexel University; Philadelphia, Pennsylvania
- Number of pages
- ix, 53 pages
- Resource Type
- Thesis
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems (1997-2026); Drexel University
- Other Identifier
- 991021890209904721