Interrupted E2F1-miR-34c-SCF negative feedback loop by hyper-methylation promotes colorectal cancer cell proliferation.
Interrupted E2F1-miR-34c-SCF negative feedback loop by hyper-methylation promotes colorectal cancer cell proliferation.
复制标题
高甲基化中断 E2F1-miR-34c-SCF 负反馈环促进结直肠癌细胞增殖
DOI：
10.1042/bsr20150290
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发表时间：
2015-12-24
影响因子：
4
通讯作者：
Zhou D
中科院分区：
文献类型：
--
作者：
Yang S;Wu B;Sun H;Ji F;Sun T;Zhao Y;Zhou D
E2 F1促进miR-34 c的转录，从而减少其靶向干细胞因子（SCF）并抑制结直肠癌（CRC）细胞增殖。而SCF增加了E2 F1的产生，表明存在E2 F1-miR-34 c-SCF负反馈环，该环被CRC细胞中miR-34 c启动子的超甲基化打断。
E2F1 promoted miR-34c transcription which reduced its target stem cell factor (SCF) and inhibited colorectal cancer (CRC) cell proliferation. While, SCF increased E2F1 production, suggesting an existence of E2F1-miR-34c-SCF negative feedback loop, which was interrupted by hyper-methylation of miR-34c promoter in CRC cells.