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- W3083857553 abstract "Lung cancer is the leading cause of cancer mortality worldwide. In particular,tumor metastasis is the most life-threatening event of lung cancer patients. More and more effective drugs for clinical use in cancer therapy have been developed up to now. However,the drug resistance is always occurred after drug treatment for a long time. Therefore,how to conquer the drug resistance during drug treatment is an important issue. Our preliminary result show that over expression of ubiquitin-specific peptidase 24 (USP24),a deubiquitinase,causes the cell apoptosis and abnormal mitosis progression,implying that USP24 might be involved in genomic instability. Therefore,we hypothesize that USP24 might induce genomic instability and drug resistance through mediating DNA damage repair activity. Our previous study indicated that increase in USP24 level in lung cancer facilitates lung cancer metastasis. Our recent study found that higher USP24 level was found in tumor-associated microenvironment (TAM) than surrounding lung cancer cells in lung cancer patient specimens. USP24 level was significantly increased in M2-macrophages. Knockdown of USP24 in M2-macrophages decreased the migratory and chemotactic activity of lung cancer cells and angiogenetic ability of human umbilical vein endothelial cells (HUVEC) induced by M2-derived conditioned medium. In vivo experiments also showed USP24 knockdown decreased M2-macrophages induced lung cancer cells metastasis and angiogenesis. IL-6 mRNA and protein levels were significantly decreased in USP24 knockdown M2-macrophages and lung cancer cells. IL-6 replenishment can rescue migratory and chemotactic ability of conditioned medium derived from USP24 knockdown M2-macrophages,suggesting that increase in USP24 in M2-macrophages induce the metastasis activity of lung through promoting IL-6 expression. To address the molecular mechanism of how USP24 regulated IL-6 in M2-macrophage and lung cancer cells, we found that USP24 stabilized p300, thereby increased the transcriptional activity of IL-6. USP24 could also decreased DNMT1 and Ikapa-B levels through stabilizing beta-TrCP and resulted in upregulated IL-6. Metastatic cytokines in tumor-associated microenvironment are important for cancer progression,in this study,we provide the direct evidence to support that USP24 increased in M2-macrophages and lung cancer cells positive regulates the metastasis of lung cancer through enhancing the IL-6 expression, which might be beneficial for the drug development for cancer therapy in the future." @default.
- W3083857553 created "2020-09-14" @default.
- W3083857553 creator A5045495656 @default.
- W3083857553 date "2018-01-01" @default.
- W3083857553 modified "2023-10-16" @default.
- W3083857553 title "USP24 Induces IL-6 in Tumor-associated Microenvironment through Stabilizing p300 and beta-TrCP to Promote the Malignancy of Lung Cancer" @default.
- W3083857553 doi "https://doi.org/10.1254/jpssuppl.wcp2018.0_po3-7-24" @default.
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