Epigenetic Dysregulation of PDX1 Drives Prostate Cancer Progression

BUFFALO, NY – April 15, 2026 – A new paper was in Volume 17 of Oncotarget on March 31, 2026, titled “Epigenetic dysregulation and biological function of PDX1 in prostate cancer.” The study was led by first author Tayo A. Adeyika and corresponding author Bernard Kwabi-Addo from Howard University, Washington, DC. The team explored the role of the pancreatic and duodenal homeobox 1 (PDX1) gene in prostate cancer, with a focus on its epigenetic regulation and biological function. Their analysis identified PDX1 as differentially hypermethylated in prostate cancer tissues compared to normal prostate samples, alongside a paradoxical increase in protein expression in tumor tissues. Experiments in prostate cancer cell lines showed that PDX1 overexpression significantly enhanced cell proliferation and migration, while knockdown of PDX1 suppressed these tumor-associated behaviors. These findings point to a clear role for PDX1 in promoting aggressive cancer phenotypes. The work further shows that PDX1 regulates key metabolic, inflammatory, and epithelial–mesenchymal transition (EMT) pathways, including genes such as INSR, IGF1R, TWIST1, and SNAI1. Notably, these effects were more pronounced under high-glucose conditions, suggesting a link between metabolic state and prostate cancer progression. “Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways.” The authors conclude that PDX1 may represent a potential therapeutic target, particularly in the context of metabolic disorders such as obesity and diabetes, which are known to influence prostate cancer risk and progression. Their findings provide new insight into the interplay between epigenetics, metabolism, and tumor biology in prostate cancer. DOI - Correspondence to - Bernard Kwabi-Addo - bkwabi-addo@howard.edu Abstract video - Sign up for free Altmetric alerts about this article -

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