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HDAC inhibitor suppresses proliferation and invasion of breast cancer cells through regulation of miR-200c targeting CRKL

机译:HDAC抑制剂通过调节miR-200c靶向crkl来抑制乳腺癌细胞的增殖和侵袭

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Although histone deacetylase (HDAC) inhibitors have been shown to effectively induce the inhibition of proliferation and migration in breast cancer, the anticancer mechanism remains poorly understood. Our studies show that miR-200c was significantly downregulated in breast cancer cell lines compared to normal cell lines and inversely correlated with the levels of class Ha HDACs and CRKL. HDAC inhibitors and the ectopic expression of miR-200c as tumor suppressors inhibited the proliferation, invasion, and migration of breast cancer cells by downregulating CRKL. These results indicate that the anticancer mechanism of HDAC inhibitor was realized partially by regulating miR-200c via CRKL targeting. Our findings suggest that the HDAC-miR200c-CRKL signaling axis could be a novel diagnostic marker and potential therapeutic target in breast cancer. (C) 2017 Elsevier Inc. All rights reserved.
机译:虽然已显示组蛋白脱乙酰酶(HDAC)抑制剂有效诱导乳腺癌中增殖和迁移的抑制,但抗癌机制仍然明白。 我们的研究表明,与正常细胞系相比,miR-200c在乳腺癌细胞系中显着下调,并与HA HDACS和CRK1的水平反向相关。 随着肿瘤抑制剂,MIR-200c的HDAC抑制剂和异位表达通过下调CRK1来抑制乳腺癌细胞的增殖,侵袭和迁移。 这些结果表明,通过CRK1靶向调节miR-200c,部分地实现了HDAC抑制剂的抗癌机制。 我们的研究结果表明,HDAC-MIR200C-CRKL信号轴可能是一种新型诊断标志物和乳腺癌的潜在治疗靶标。 (c)2017年Elsevier Inc.保留所有权利。

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