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Creation Date
4-24-2025
Description
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a median survival time of 10-12 months. Therefore, it is crucial to investigate the molecular mechanism underlying PDAC initiation and progression. Metabolic stress occurs in various cancer types, including PDAC, due to the limited availability of nutrients and high metabolic demands. The present study aims to investigate the possible survival molecular mechanisms of cancer cells under metabolic stress conditions. Using nutrient starvation models, immunoblotting, and gene expression analysis, we are investigating how cancer cells respond to glycometabolic stress. Our preliminary data indicate cancer cells compensate by going into cell cycle arrest and inducing autophagy. In addition, we are exploring the role of lactate in the epigenetic reprogramming of cancer cells. PDAC manifests a high rate of glucose metabolism and is characterized by an increase in lactate production (Warburg effect). We hypothesize that lactate can serve as a vital metabolic regulator of gene expression. Our preliminary findings indicate that cancer cells utilize lactate as a regulatory molecule, modifying histones and potentially altering transcriptional programs and protein production to enhance survival. Understanding the functional significance of lactylation in cancer cells could provide new insights into tumor adaptation mechanisms and reveal potential therapeutic targets.
Keywords
SWOSU Research Fair, Research and Scholarly Activity Fair, Scholarly Activity, Research, Student Research, Research Fair