Cakici, CagriDaylan, BenayUnluer, Ruveyde SafiyeEmekli-Alturfan, EbruAyla, SuleGozel, Hilal ErenYigitbasi, TurkanTıbbi Biyoloji Anabilim Dalı / Department of Medical Biology2024-05-252024-05-25202401837-966410.7150/jca.862832-s2.0-85185716416https://doi.org/10.7150/jca.86283https://hdl.handle.net/20.500.14517/1161Eren Gozel, Hilal/0000-0001-6026-6052;Increased LDH-A activity promotes tumor growth, migration, invasion, and metastasis. This study aimed to investigate the effects of the combination of LDH-A inhibitor and Docetaxel on apoptosis and epithelial-mesenchymal transition (EMT) in the murine prostate cancer (PCa) model. The prostate cancer murine model was developed subcutaneously in 50 male B57CL/6 mice using the Tramp -C2 prostate cancer cell line. From the tumor tissue samples, apoptosis analysis was performed using TUNEL staining, and EMT was investigated using western blot and qPCR. Hematoxylin-eosin staining (HE) and Periodic acid-Schiff staining were used to histopathologically examine liver and kidney tissues. Lactate levels revealed that the Warburg effect was reversed with the LDH-A inhibitor. Both serum and tumor tissue apoptosis increased, and tumor sizes reduced in PCa+LDH-A inhibitor + Docetaxel treatment groups (p<0.05). The combination of LDH-A inhibitor and Docetaxel inhibited EMT mechanism by causing a decrease in Snail, Slug, Twist, and HIF-1 alpha expressions as well as a decrease in N-cadherin and an increase in E-cadherin levels. Reprogramming glucose metabolism with an LDH-A inhibitor can increase the effectiveness of Docetaxel on apoptosis and metastasis mechanisms in PCa.eninfo:eu-repo/semantics/openAccessProstate cancerApoptosisEMTLDH-A inhibitorWarburg effectArticleQ2Q1153590602WOS:00116729790000438213726