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Curcumin suppressed the prostate cancer by inhibiting JNK pathways via epigenetic regulation

机译:通过通过表观遗传调节抑制JNK途径抑制姜黄素抑制前列腺癌

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Abstract Curcumin is a component of turmeric and is isolated from the rhizomes of the plant Curcuma longa . Curcumin was reported to have therapeutic effects on prostate cancer. Yet the molecular mechanism of curcumin remains unclear. In this study, mouse prostate cancer xenograft model was established and subjected to curcumin treatment. GST‐c‐Jun pull down kinase assays were performed to study the phospho‐c‐Jun level. Cell Counting Kit‐8 assay kit was utilized to detect the cell viability. Immunoblotting and qRT‐PCR were performed for target gene expression analysis. Curcumin inhibited growth of prostate cancer in vivo as well as promoted apoptosis of LNCaP cells in vitro. Curcumin inhibited JNK pathway and repressed H3K4me3 in LNCaP cells. Combined use of curcumin and JQ‐1 inhibited the prostate cancer efficiently. In conclusion, curcumin inhibits JNK pathway and plays a role in epigenetic regulation of prostate cancer cells by repressing H3K4me3.
机译:摘要姜黄素是姜黄的组成部分,并与植物姜黄Longa的根茎隔离。 据报道姜黄素对前列腺癌进行治疗作用。 然而,姜黄素的分子机制仍不清楚。 在这项研究中,建立了小鼠前列腺癌异种移植模型并进行姜黄素处理。 进行GST-C-JUM拉伸激酶测定以研究磷酸-C-Jun水平。 使用细胞计数试剂盒-8测定试剂盒检测细胞活力。 对靶基因表达分析进行免疫印迹和QRT-PCR。 姜黄素抑制体内前列腺癌的生长,以及在体外促进LNCAP细胞的凋亡。 姜黄素抑制JNK途径和LNCAP细胞中的抑制H3K4ME3。 姜黄素和JQ-1的结合使用有效抑制前列腺癌。 总之,姜黄素抑制JNK途径,并通过压制H3K4ME3在前列腺癌细胞的表观遗传调节中起作用。

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