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@#To explore the mechanisms by which AKR1C3 induces tumor resistance, human breast cancer cell strain MCF-7/DOX resistant to doxorubicin, MCF-7/ AKR1C3 cells for overexpression of AKR1C3 and MCF-7/DOX-KD cells for knockdown of AKR1C3 in MCF-7/DOX cells were established. Western blot analysis found that AKR1C3 was expressed at a higher level in MCF-7/DOX than MCF-7 wild type cells. Similarly, CCK-8 and DAPI confirmed that MCF-7/ AKR1C3 cells were more resistant to DOX than AKR1C3 wild types as the IC50 was increased 6 times in MCF-7/AKR1C3 cells more than in AKR1C3 wild type cells. Meanwhile, colony formation ability was also enhanced after AKR1C3 was over-expressed in MCF-7 cells.Cytoplasmic/nuclear separation analysis and IF further found that β-catenin nuclear translocation mediated by AKR1C3 was the main reason contributing to the occurrence of DOX-resistant breast cancer cells. β-catenin inhibitor, XAV939, could reverse the AKR1C3 induced doxorubicin resistance in MCF-7 cells.Results indicated that AKR1C3 could be a potential therapeutic target in breast cancer cells.
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Objective To evaluate the significance of the expression level of aldo-keto reductase family 1 member C3(AKR1C3) for esophageal carcinoma patients treated with radiotherapy.Methods The clinical data of 28 patients with locally advanced esophageal carcinoma treated with radiotherapy alone was retrospectively analyzed, and the expression level of AKR1C3 was detected by immunohistochemistry.Statistical analysis was performed using SAS 8 statistical software, P<0.05 was considered statistically significant difference.Results The expression level of AKR1C3 was different in esophageal carcinoma patients at different levels of differentiation.The level of AKR1C3 expression was negatively correlated with efficacy of radiotherapy (P=0.031, 95%CI 0.151-0.914).Conclusion AKR1C3 can serve as a promising biomarker of the efficacy of radiotherapy for esophageal cancer.
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BACKGROUND: Diabetes is characterized by chronic hyperglycemia, and hyperglycemia can increase reactive oxygen species (ROS) production from the mitochondrial electron transport chain. The formation of ROS in cells induces oxidative stress and activates oxidative damage-inducing genes. There is no research on the protein levels of oxidative damage-related genes AKR1C3 in human diabetic skin. We explored the expression of AKR1C3 in diabetic skin compared with normal skin tissue. OBJECTIVE: To compare the expression of AKR1C3 in normal skin versus diabetic skin. METHODS: AKR1C3 expression was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was carried out to analyze AKR1C3 expression in the 6 diabetic skin tissue samples (July 2009 to December 2011; Department of Plastic and Reconstructive Surgery at Soonchunhyang University Seoul Hospital, Seoul, Korea). RESULTS: The western blotting showed a significant reduction in AKR1C3 protein expression in diabetic skin tissue compared to normal tissue. Immunohistochemical examination of AKR1C3 showed that it was weakly expressed in all diabetic skin samples. CONCLUSION: We believe that AKR1C3 is related to diabetic skin in altered metabolic states which elevate ROS production.