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Reactivation of IGFBP7 by DNA demethylation inhibits human colon cancer cell growth in vitro.

机译:DNA去甲基化重新激活IGFBP7可抑制人结肠癌细胞的体外生长。

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BACKGROUND: The insulin-like growth factor binding protein 7 (IGFBP7) gene is regulated by DNA methylation in colon cancer, which was identified in our previous study. In this study, we examined the effects of DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) on IGFBP7 reactivation and cell biological behaviors in vitro to investigate a potential role for 5-aza-dC in treating colorectal cancer. RESULTS: 5-aza-dC treatment showed induction of IGFBP7 transcription in these cancer cells. It consequently led to inhibition of cell growth, cell cycle arrest and apoptosis, suppression of cell migration and invasion in colon cancer cell lines. METHODS: We examined the effects of 5-aza-dC on reexpression of previously silenced IGFBP7 and its global effects on cell cycle, apoptosis, migration and invasion in three colon cancer cell lines, SW620, HT29 and COLO205. CONCLUSION: Our findings indicate that 5-aza-dC may have anticancer function for colon cancer and restoration of IGFBP7 may involve in the biological effects induced by 5-aza-dC in colon cancer cell lines. These data suggest that 5-aza-dC has clinical potential in the treatment of colorectal cancer.
机译:背景:胰岛素样生长因子结合蛋白7(IGFBP7)基因受结肠癌中DNA甲基化的调控,这在我们先前的研究中已经确定。在这项研究中,我们研究了DNA甲基化抑制剂5-氮杂2'-脱氧胞苷(5-氮杂-dC)对IGFBP7活化和体外细胞生物学行为的影响,以研究5-氮杂-dC在治疗结直肠癌中的潜在作用癌症。结果:5-氮杂-dC处理显示在这些癌细胞中诱导了IGFBP7转录。因此,它导致结肠癌细胞系中细胞生长的抑制,细胞周期的阻滞和凋亡,细胞迁移的抑制和侵袭。方法:我们研究了5-氮杂-dC对先前沉默的IGFBP7的重新表达的影响及其对三个结肠癌细胞系SW620,HT29和COLO205的细胞周期,凋亡,迁移和侵袭的整体影响。结论:我们的发现表明5-氮杂-dC可能对结肠癌具有抗癌作用,而IGFBP7的恢复可能与5-氮杂-dC在结肠癌细胞系中的生物学作用有关。这些数据表明5-氮杂-dC在结直肠癌的治疗中具有临床潜力。

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