Talks
Presenting Author Academic/Professional Position
Graduate Student
Academic Level (Author 1)
Post-doc
Discipline/Specialty (Author 1)
Immunology and Microbiology
Academic Level (Author 2)
Staff
Discipline/Specialty (Author 2)
Immunology and Microbiology
Academic Level (Author 3)
Graduate Student
Academic Level (Author 4)
Graduate Student
Discipline/Specialty (Author 4)
Immunology and Microbiology
Academic Level (Author 5)
Graduate Student
Discipline/Specialty (Author 5)
Immunology and Microbiology
Presentation Type
Oral Presentation
Discipline Track
Biomedical Science
Abstract Type
Program Abstract
Abstract
Background: The emergence of drug resistance in cancer remains a significant challenge, despite significant progress in targeted therapies. Drug resistance is responsible for approximately 90% of cancer-related deaths. YBX1, an oncoprotein, has been implicated in cancer progression and resistance to treatment in several cancers, including breast and colorectal cancers. In our previous work, we demonstrated that overexpression of YBX1 contributes to increased cell survival and viability, promoting resistance to sorafenib in hepatocellular carcinoma (HCC).Sorafenib, a tyrosine kinase inhibitor, is approved for the treatment of advanced HCC. Although it provides some survival benefit, its overall effect on survival is limited, with resistance generally emerging after six months of treatment. The mechanisms underlying sorafenib resistance in HCC are not fully understood, but are believed to involve a combination of factors, such as activation of alternative signaling pathways, changes in the tumor microenvironment, genetic mutations, and altered drug metabolism.
Methods and Results: In this study, we present evidence that inhibiting YBX1 sensitizes HCC cells to sorafenib treatment. By using siRNA transfection for YBX1 inhibition, we observed a significant reduction in cell survival and an enhanced response to sorafenib, as assessed by MTT assays in HCC cell lines. Additionally, YBX1 inhibition decreased colony formation, invasion, and proliferation of HCC cells when combined with sorafenib treatment.
Conclusion: Our findings suggest that YBX1 plays a critical role in mediating sorafenib resistance, and its inhibition may represent a promising strategy for overcoming resistance, potentially improving the clinical efficacy of sorafenib in advanced HCC. Further studies are necessary to explore the therapeutic potential of combining YBX1 inhibition with sorafenib to enhance treatment outcomes in HCC patients
Recommended Citation
Kwabiah, Dennis; Nagati, Veerababu; Anaya, Yamile Abuchard; Pazzi, Gabriella Ayala; Leslie, Sophia; Bracho, Ricardo Pequeno; and Tripathi, Manish, "YBX1: A Promising Target for Enhancing Sorafenib Sensitivity in Hepatocellular Carcinoma" (2025). Research Symposium. 8.
https://scholarworks.utrgv.edu/somrs/2025/talks/8
Included in
YBX1: A Promising Target for Enhancing Sorafenib Sensitivity in Hepatocellular Carcinoma
Background: The emergence of drug resistance in cancer remains a significant challenge, despite significant progress in targeted therapies. Drug resistance is responsible for approximately 90% of cancer-related deaths. YBX1, an oncoprotein, has been implicated in cancer progression and resistance to treatment in several cancers, including breast and colorectal cancers. In our previous work, we demonstrated that overexpression of YBX1 contributes to increased cell survival and viability, promoting resistance to sorafenib in hepatocellular carcinoma (HCC).Sorafenib, a tyrosine kinase inhibitor, is approved for the treatment of advanced HCC. Although it provides some survival benefit, its overall effect on survival is limited, with resistance generally emerging after six months of treatment. The mechanisms underlying sorafenib resistance in HCC are not fully understood, but are believed to involve a combination of factors, such as activation of alternative signaling pathways, changes in the tumor microenvironment, genetic mutations, and altered drug metabolism.
Methods and Results: In this study, we present evidence that inhibiting YBX1 sensitizes HCC cells to sorafenib treatment. By using siRNA transfection for YBX1 inhibition, we observed a significant reduction in cell survival and an enhanced response to sorafenib, as assessed by MTT assays in HCC cell lines. Additionally, YBX1 inhibition decreased colony formation, invasion, and proliferation of HCC cells when combined with sorafenib treatment.
Conclusion: Our findings suggest that YBX1 plays a critical role in mediating sorafenib resistance, and its inhibition may represent a promising strategy for overcoming resistance, potentially improving the clinical efficacy of sorafenib in advanced HCC. Further studies are necessary to explore the therapeutic potential of combining YBX1 inhibition with sorafenib to enhance treatment outcomes in HCC patients
