Presentation Type
Oral/Paper Presentation
Abstract
Breast cancer accounts for approximately 297,500 cases annually in the United States, leading to over 43,000 fatalities. These deaths occur due to cancer's ability to bypass the normal cell cycle, proliferating uncontrollably and metastasizing throughout the body. Notably, over 75% of breast cancer-related deaths are attributed to metastases. The hallmark of altered cellular metabolism enables cancer cells to enhance fat metabolism alongside glycolysis, driving increased tumor aggressiveness and higher metastatic rates. Currently, no FDA-approved drugs directly target metastases or prevent migrating cancer cells. Consequently, inhibiting fat metabolism presents a potential strategy to reduce metastases and cancer cell migration; however, existing fat metabolism inhibitors exhibit significant toxicity, preventing clinical translation.
Our previous research identified Valerobetaine (VB), a non-toxic microbial metabolite, as a promising inhibitor of fat metabolism. Initial experiments demonstrated that VB reduced MCF-7 breast cancer cell migration under fatty acid supplementation using scratch assays. These studies confirmed that VB mitigates the pro-migratory effects associated with enhanced fat metabolism. Further research investigated VB’s mechanism of action, hypothesizing its function through carnitine-dependent pathways. Using treatment groups with carnitine supplementation and conducting scratch assays, we observed that VB’s inhibitory effect on migration was reversed, implicating the carnitine shuttle in its mechanism. These findings highlight VB’s potential as a co-therapeutic for mitigating metastatic behavior in breast cancer, supporting its future clinical application.
Faculty Mentor
Dr. Joshua A. Owens
Recommended Citation
Birdwell, Audrey, "Investigating Carnitine-Dependent Mechanisms of Valerobetaine in Breast Cancer Migration Inhibition" (2025). Student Scholar Symposium. 43.
https://digitalcollections.lipscomb.edu/student_scholars_symposium/2025/Full_schedule/43
Included in
Investigating Carnitine-Dependent Mechanisms of Valerobetaine in Breast Cancer Migration Inhibition
Breast cancer accounts for approximately 297,500 cases annually in the United States, leading to over 43,000 fatalities. These deaths occur due to cancer's ability to bypass the normal cell cycle, proliferating uncontrollably and metastasizing throughout the body. Notably, over 75% of breast cancer-related deaths are attributed to metastases. The hallmark of altered cellular metabolism enables cancer cells to enhance fat metabolism alongside glycolysis, driving increased tumor aggressiveness and higher metastatic rates. Currently, no FDA-approved drugs directly target metastases or prevent migrating cancer cells. Consequently, inhibiting fat metabolism presents a potential strategy to reduce metastases and cancer cell migration; however, existing fat metabolism inhibitors exhibit significant toxicity, preventing clinical translation.
Our previous research identified Valerobetaine (VB), a non-toxic microbial metabolite, as a promising inhibitor of fat metabolism. Initial experiments demonstrated that VB reduced MCF-7 breast cancer cell migration under fatty acid supplementation using scratch assays. These studies confirmed that VB mitigates the pro-migratory effects associated with enhanced fat metabolism. Further research investigated VB’s mechanism of action, hypothesizing its function through carnitine-dependent pathways. Using treatment groups with carnitine supplementation and conducting scratch assays, we observed that VB’s inhibitory effect on migration was reversed, implicating the carnitine shuttle in its mechanism. These findings highlight VB’s potential as a co-therapeutic for mitigating metastatic behavior in breast cancer, supporting its future clinical application.