Talks
Presenting Author Academic/Professional Position
Karla Perez
Academic Level (Author 1)
Post-doc
Discipline/Specialty (Author 1)
Cancer and Immunology
Academic Level (Author 2)
Graduate Student
Discipline/Specialty (Author 2)
Cancer and Immunology
Academic Level (Author 3)
Faculty
Discipline/Specialty (Author 3)
Cancer and Immunology
Academic Level (Author 4)
Faculty
Discipline/Specialty (Author 4)
Cancer and Immunology
Academic Level (Author 5)
Faculty
Discipline/Specialty (Author 5)
Cancer and Immunology
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Non-alcoholic fatty liver disease (NAFLD) is a progressive metabolic disorder affecting the liver, which can lead to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma (HCC). Recent transcriptomic analyses have identified pathways that may be critical in disease progression and could serve as biomarkers or therapeutic targets. However, those studies were limited to transcripts encoding proteins, neglecting over 70% of the genome, which is composed of non-coding transcripts. Therefore, it is essential to reanalyze the transcriptomic data in an unbiased manner from normal, NAFLD, and NASH patient liver samples to identify transcripts with limited coding potential. These may show very specific expression patterns and open up new therapeutic options.
Methods: We extracted whole transcriptomic data from over 200 patients with NAFLD or NASH, and analyzed them to identify all transcripts, including both coding and non-coding types, that are differentially regulated compared to normal liver tissue. Additionally, since many long non-coding transcripts have limited functional studies available, we employed the Genomic Regions Enrichment of Annotations Tool (GREAT) to understand the functional relevance of these non-coding transcripts. GREAT is a tool designed for functional analysis of genomic regions, linking them to biologically meaningful terms.
Results: We identified numerous genes that were either upregulated or downregulated, with limited coding potential, which overlapped or were specific to NAFLD or NASH. Among the upregulated noncoding transcripts, 297 were common to both NAFLD and NASH, while 40 were unique to NAFLD and 79 were unique to NASH. Similarly, for downregulated non-coding transcripts, there were 371 common transcripts, 77 unique to NAFLD, and 116 unique to NASH. Additionally, GREAT analyses revealed several pathways associated with these transcripts, which may provide insights into predisposed conditions that could exacerbate disease progression.
Conclusion: Studying the historically overlooked transcripts may provide new diagnostic and therapeutic targets that could aid in controlling this disease, which is prevalent in Texas including the Rio Grande Valley.
Acknowledgements: S.S.G. is a CPRIT Scholar in Cancer Research. S.S.G. is supported by NIH 1R16GM149497 and The American Cancer Society (RSG-22-170-01-RMC) grants.
Presentation Type
Talk
Recommended Citation
Perez, Karla; Delgadillo, Frida; Dhandayuthapani, Subramanian; Yallapu, Murali; Chauhan, Subhash; Ramos, Enrique; and Gadad, Shrikanth, "Analyses of NAFLD And NASH Transcriptome Reveal Unique Differentially Regulated RNAs and Cellular Pathways" (2025). Research Colloquium. 6.
https://scholarworks.utrgv.edu/colloquium/2025/talks/6
Included in
Analyses of NAFLD And NASH Transcriptome Reveal Unique Differentially Regulated RNAs and Cellular Pathways
Background: Non-alcoholic fatty liver disease (NAFLD) is a progressive metabolic disorder affecting the liver, which can lead to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma (HCC). Recent transcriptomic analyses have identified pathways that may be critical in disease progression and could serve as biomarkers or therapeutic targets. However, those studies were limited to transcripts encoding proteins, neglecting over 70% of the genome, which is composed of non-coding transcripts. Therefore, it is essential to reanalyze the transcriptomic data in an unbiased manner from normal, NAFLD, and NASH patient liver samples to identify transcripts with limited coding potential. These may show very specific expression patterns and open up new therapeutic options.
Methods: We extracted whole transcriptomic data from over 200 patients with NAFLD or NASH, and analyzed them to identify all transcripts, including both coding and non-coding types, that are differentially regulated compared to normal liver tissue. Additionally, since many long non-coding transcripts have limited functional studies available, we employed the Genomic Regions Enrichment of Annotations Tool (GREAT) to understand the functional relevance of these non-coding transcripts. GREAT is a tool designed for functional analysis of genomic regions, linking them to biologically meaningful terms.
Results: We identified numerous genes that were either upregulated or downregulated, with limited coding potential, which overlapped or were specific to NAFLD or NASH. Among the upregulated noncoding transcripts, 297 were common to both NAFLD and NASH, while 40 were unique to NAFLD and 79 were unique to NASH. Similarly, for downregulated non-coding transcripts, there were 371 common transcripts, 77 unique to NAFLD, and 116 unique to NASH. Additionally, GREAT analyses revealed several pathways associated with these transcripts, which may provide insights into predisposed conditions that could exacerbate disease progression.
Conclusion: Studying the historically overlooked transcripts may provide new diagnostic and therapeutic targets that could aid in controlling this disease, which is prevalent in Texas including the Rio Grande Valley.
Acknowledgements: S.S.G. is a CPRIT Scholar in Cancer Research. S.S.G. is supported by NIH 1R16GM149497 and The American Cancer Society (RSG-22-170-01-RMC) grants.
