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• W2255169021 abstract "Acute myeloid leukemia is the majority type presented in leukemia patients. Forcing malignant cells to undergo differentiation is 1 strategy for acute myeloid leukemia therapy. However, the failure of acute myeloid leukemia patients to achieve remission as a result of drug resistance remains a challenge. In this study, we found that the abundances of the proinflammatory cytokine IL-18 and its receptor (IL-18R) correlated with the occurrence of drug resistance in AML patients during standard treatment. Cyclooxygenase 2 (COX-2) has been suggested to have an antiapoptotic role in chemoresistant cancer cells. IL-18 treatment resulted in an increase in COX-2 expression through the post-transcriptional regulation of COX-2 mRNA in differentiated U937 cells and showed antiapoptotic activity in U937 and THP-1 cells. Two RNA-binding proteins, human antigen R and insulin-like growth factor mRNA-binding protein 3, mediated the stabilization of COX-2 mRNA. IL-18 induced the shuttling of human antigen R and insulin-like growth factor mRNA-binding protein 3 from the nucleus to the cytoplasm and facilitated their interaction; subsequently, this complex bound to the 3' untranslated region of COX-2 mRNA and affected its stability. We demonstrated further that JNK and/or ERK1/2 regulated human antigen R nucleocytoplasmic shuttling, mediating IL-18 stabilization of cyclooxygenase 2 mRNA." @default.
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• W2255169021 date "2015-09-04" @default.
• W2255169021 modified "2023-10-18" @default.
• W2255169021 title "IL-18-induced interaction between IMP3 and HuR contributes to <i>COX-2</i> mRNA stabilization in acute myeloid leukemia" @default.
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• W2255169021 doi "https://doi.org/10.1189/jlb.2a0414-228rr" @default.
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