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Abstract
Background: The most prevalent type of liver cancer is hepatocellular carcinoma (HCC), and socioeconomic and health disparities have a major impact on both its incidence and fatality rates. HCC rates are typically greater in areas with poor access to healthcare, high obesity rates, and a high frequency of infectious diseases. Because of risk factors include diabetes, non-alcoholic fatty liver disease (NAFLD), and Hepatitis B and C, HCC is particularly common in the Rio Grande Valley (RGV). The burden of HCC in this underprivileged area is made worse by McAllen, Texas, which regrettably holds the distinction of being the most obese city in the US. Patient outcomes are greatly impacted by late-stage diagnoses, which are frequently the result of limited access to screening and early detection. Improving early detection and treatment of HCC requires an understanding of the molecular pathways underlying the disease, including medication resistance. Resistance to sorafenib, the first-line tyrosine kinase inhibitor (TKI) used for advanced HCC, and Y-Box Binding Protein 1 (YBX1) are important factors in the progression of HCC. By interacting with microRNAs and non-coding RNAs, the 324-amino acid protein YB-1, which is a member of the Cold Shock Domain (CSD) protein family, helps control the translation of mRNA. Despite sorafenib's efficacy, resistance frequently arises, and little is known about the underlying causes of this resistance.
Methods: ATCC methods were used to cultivate the HCC cell line SK-Hep1. Abmgood produced lentiviral overexpression plasmids for YBX1 that included a puromycin selection marker and GFP. Western blot and RT-PCR were used to confirm the levels of YBX1 expression. To describe phenotypic changes, functional experiments were conducted, including invasion, migration, proliferation, colony formation, and Xcelligence impedance analysis. To find kinase pathways impacted by YBX1, a phosphoproteome array was utilized.
Results: According to an analysis of The Cancer Genome Atlas (TCGA), YBX1 expression is substantially higher in HCC tumors than in normal tissues and is associated with poor survival, metastasis, and disease progression. YBX1 overexpression promoted colony formation, invasion, migration, and proliferation, among other carcinogenic tendencies, in vitro. YBX1 knockdown (KD), on the other hand, decreased these behavioral traits. Xcelligence impedence experiments verified that YBX1-overexpressing cells proliferated more, whereas knockdown cells grew at slower rates. In HCC cells, phosphoproteome research revealed a number of kinases that are YBX1 regulated. Additional pathway analysis is being conducted to clarify their functions in drug resistance.
Conclusion and Future Directions: GFP-expressing SK-Hep1 cell lines with stable YBX1 overexpression and knockdown have been effectively created and characterized. These models show how YBX1 plays a crucial part in encouraging carcinogenic traits in HCC. Based on our results we procured certain kinase activators and inhibitors which were evaluated through literature and purchased for additional studies in order to obtain understanding of the YBX1-regulated signaling pathways resulting in sorafenib resistance. The goal of ongoing proteomic research is to better understand the proteins and pathways linked to YBX1, with an emphasis on kinase regulation. These results may help direct the development of tailored therapies to overcome resistance in HCC and advance our understanding of the processes underlying sorafenib resistance.
Recommended Citation
Abuchard Anaya, Yamile; Ayala Pazzi, Ana; Kwabiah, Dennis; Nagati, Veerababu; Pequeno Bracho, Ricardo; Doxtater, Kyle; Chauhan, Subhash C.; and Tripathi, Manish K., "Novel Signaling Pathways Involved in YBX1 role in Hepatocellular Carcinoma" (2025). Research Symposium. 175.
https://scholarworks.utrgv.edu/somrs/2025/posters/175
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Biological Phenomena, Cell Phenomena, and Immunity Commons, Medical Molecular Biology Commons, Other Medical Sciences Commons
Novel Signaling Pathways Involved in YBX1 role in Hepatocellular Carcinoma
Background: The most prevalent type of liver cancer is hepatocellular carcinoma (HCC), and socioeconomic and health disparities have a major impact on both its incidence and fatality rates. HCC rates are typically greater in areas with poor access to healthcare, high obesity rates, and a high frequency of infectious diseases. Because of risk factors include diabetes, non-alcoholic fatty liver disease (NAFLD), and Hepatitis B and C, HCC is particularly common in the Rio Grande Valley (RGV). The burden of HCC in this underprivileged area is made worse by McAllen, Texas, which regrettably holds the distinction of being the most obese city in the US. Patient outcomes are greatly impacted by late-stage diagnoses, which are frequently the result of limited access to screening and early detection. Improving early detection and treatment of HCC requires an understanding of the molecular pathways underlying the disease, including medication resistance. Resistance to sorafenib, the first-line tyrosine kinase inhibitor (TKI) used for advanced HCC, and Y-Box Binding Protein 1 (YBX1) are important factors in the progression of HCC. By interacting with microRNAs and non-coding RNAs, the 324-amino acid protein YB-1, which is a member of the Cold Shock Domain (CSD) protein family, helps control the translation of mRNA. Despite sorafenib's efficacy, resistance frequently arises, and little is known about the underlying causes of this resistance.
Methods: ATCC methods were used to cultivate the HCC cell line SK-Hep1. Abmgood produced lentiviral overexpression plasmids for YBX1 that included a puromycin selection marker and GFP. Western blot and RT-PCR were used to confirm the levels of YBX1 expression. To describe phenotypic changes, functional experiments were conducted, including invasion, migration, proliferation, colony formation, and Xcelligence impedance analysis. To find kinase pathways impacted by YBX1, a phosphoproteome array was utilized.
Results: According to an analysis of The Cancer Genome Atlas (TCGA), YBX1 expression is substantially higher in HCC tumors than in normal tissues and is associated with poor survival, metastasis, and disease progression. YBX1 overexpression promoted colony formation, invasion, migration, and proliferation, among other carcinogenic tendencies, in vitro. YBX1 knockdown (KD), on the other hand, decreased these behavioral traits. Xcelligence impedence experiments verified that YBX1-overexpressing cells proliferated more, whereas knockdown cells grew at slower rates. In HCC cells, phosphoproteome research revealed a number of kinases that are YBX1 regulated. Additional pathway analysis is being conducted to clarify their functions in drug resistance.
Conclusion and Future Directions: GFP-expressing SK-Hep1 cell lines with stable YBX1 overexpression and knockdown have been effectively created and characterized. These models show how YBX1 plays a crucial part in encouraging carcinogenic traits in HCC. Based on our results we procured certain kinase activators and inhibitors which were evaluated through literature and purchased for additional studies in order to obtain understanding of the YBX1-regulated signaling pathways resulting in sorafenib resistance. The goal of ongoing proteomic research is to better understand the proteins and pathways linked to YBX1, with an emphasis on kinase regulation. These results may help direct the development of tailored therapies to overcome resistance in HCC and advance our understanding of the processes underlying sorafenib resistance.
