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Chlorogenic-induced inhibition of non-small cancer cells occurs through regulation of histone deacetylase 6

机译:通过组蛋白脱乙酰酶6的调节,发生绿原诱导的非小癌细胞的抑制

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摘要

Chlorogenic acid (CGA), an ester with various pharmacological effects, is important in cancer therapy. However, the specific antitumor mechanism of CGA is not entirely clear, especially with respect to its suppression of non-small cell lung cancer (NSCLC). The present study was carried out to assess the effect of CGA on NSCLC, and the mechanism involved. Cell viability assay and colony formation assay revealed that CGA blocked the proliferative capacity of NSCLC cells in vitro. Results from the migration assay suggested that CGA also inhibited the migration of A549 cells. Other assays further revealed that CGA strongly and selectively inhibited histone deacetylase 6 (HDAC6) activity and suppressed the activity of matrix metalloproteinase-2 (MMP-2) through decreased expression of Ac-NF-kappa B. Tumorigenicity assay showed that CGA also inhibited the proliferation and metabolism of NSCLC in vivo. These results indicate that CGA significantly suppresses the proliferation of NSCLC by regulating the activity of histone deacetylase 6.
机译:绿原酸(CGA),具有各种药理作用的酯,在癌症治疗中是重要的。然而,CGA的特异性抗肿瘤机制不完全清楚,特别是关于其抑制非小细胞肺癌(NSCLC)。进行本研究以评估CGA对NSCLC的影响,以及所涉及的机制。细胞活力测定和菌落形成测定显示CGA在体外阻断了NSCLC细胞的增殖能力。迁移检测结果表明CGA还抑制了A549细胞的迁移。其他测定进一步揭示CGA强烈且选择性地抑制组蛋白脱乙酰酶6(HDAC6)活性,并通过减少AC-NF-Kappa B.致致瘤性测定表达CGA也抑制了基质金属蛋白酶-2(MMP-2)的活性。CGA也抑制了NSCLC在体内的增殖和新陈代谢。这些结果表明,CGA通过调节组蛋白脱乙酰酶6的活性显着抑制NSCLC的增殖。

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