Posters
Presenting Author Academic/Professional Position
Post-doc
Academic Level (Author 1)
Post-doc
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Immunology and Microbiology
Academic Level (Author 2)
Faculty
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Immunology and Microbiology
Academic Level (Author 3)
Staff
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Immunology and Microbiology
Presentation Type
Oral Presentation
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Community/Public Health
Abstract Type
Research/Clinical
Abstract
Background: Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to limited therapeutic options and a lack of early diagnostic markers. Recent studies have highlighted the elevated expression of mucin 13 as a potential oncogene and predictive biomarker in various cancers. However, its role in the development and progression of HCC remains largely unexplored. This study aimed to investigate the expression of mucin 13 in a chemically induced model of hepatocellular carcinoma.
Methodology: We employed a chemically induced model of hepatocellular carcinoma in Male Wistar rats using diethyl nitrosamine and 2-acetylaminofluorene. Serum and tissue samples were collected at regular intervals to assess the progression of liver cancer stages. Immunohistochemistry and in situ hybridization were performed on formalin-fixed, paraffin-embedded tissues. To explore the interaction between mucin 13 and DEN, molecular docking studies were conducted.
Results: Histopathological analysis confirmed the presence of hepatocellular adenoma in the treatment group. Biochemical assessment revealed progressive increases in serum levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, indicating liver damage progression. Notably, there was a significant increase in mucin 13 expression across the consecutive stages of hepatocellular carcinoma, with enhanced nuclear localization observed in the treated group compared to controls. Additionally, in situ hybridization analysis indicated a decrease in miR-145, which inversely correlate with mucin 13 expression. Molecular docking studies further revealed that DEN binds to mucin 13 with high affinity, suggesting a role in its stabilization.
Conclusion: Our findings indicate that the expression of mucin 13 is closely linked to hepatocarcinogenesis and may serve as a candidate predictive biomarker for HCC. Further investigation into the mechanisms underlying this relationship could provide insights into its potential as a therapeutic target and diagnostic tool.
Recommended Citation
Malik, Shabnam; Sikander, Mohammed; Zubieta, Daniel; Khan, Parvez; Yallapu, Murali M.; Katare, Deepshikha P.; Jain, S.K; Jaggi, Meena; and Chauhan, Subhash C., "Studying the Significance of MUC13 in Hepatocellular Carcinoma" (2025). Research Symposium. 145.
https://scholarworks.utrgv.edu/somrs/2025/posters/145
Studying the Significance of MUC13 in Hepatocellular Carcinoma
Background: Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to limited therapeutic options and a lack of early diagnostic markers. Recent studies have highlighted the elevated expression of mucin 13 as a potential oncogene and predictive biomarker in various cancers. However, its role in the development and progression of HCC remains largely unexplored. This study aimed to investigate the expression of mucin 13 in a chemically induced model of hepatocellular carcinoma.
Methodology: We employed a chemically induced model of hepatocellular carcinoma in Male Wistar rats using diethyl nitrosamine and 2-acetylaminofluorene. Serum and tissue samples were collected at regular intervals to assess the progression of liver cancer stages. Immunohistochemistry and in situ hybridization were performed on formalin-fixed, paraffin-embedded tissues. To explore the interaction between mucin 13 and DEN, molecular docking studies were conducted.
Results: Histopathological analysis confirmed the presence of hepatocellular adenoma in the treatment group. Biochemical assessment revealed progressive increases in serum levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, indicating liver damage progression. Notably, there was a significant increase in mucin 13 expression across the consecutive stages of hepatocellular carcinoma, with enhanced nuclear localization observed in the treated group compared to controls. Additionally, in situ hybridization analysis indicated a decrease in miR-145, which inversely correlate with mucin 13 expression. Molecular docking studies further revealed that DEN binds to mucin 13 with high affinity, suggesting a role in its stabilization.
Conclusion: Our findings indicate that the expression of mucin 13 is closely linked to hepatocarcinogenesis and may serve as a candidate predictive biomarker for HCC. Further investigation into the mechanisms underlying this relationship could provide insights into its potential as a therapeutic target and diagnostic tool.
