结直肠癌是一种常见且恶性的癌症，具有高发病率和预后差。本研究旨在探讨MT1G在结直肠癌中的调节作用及其分子机制。采用RT-qPCR和Western blot评估MT1G、c-MYC和p53的表达。通过CCK-8和BrdU合成实验测量MT1G过表达对HCT116和LoVo细胞增殖能力的影响。此外，采用Transwell伤口愈合和流式细胞术评估HCT116和LoVo细胞的侵袭和迁移能力以及凋亡水平。此外，利用荧光素酶报告试验评估p53启动子区域的活性。研究发现，在人类结直肠癌细胞系中MT1G基因在mRNA和蛋白质水平上的表达大幅降低，特别是在HCT116和LoVo细胞系中。转染后发现，MT1G过表达可抑制HCT116和LoVo细胞的增殖、迁移和侵袭，但促进其凋亡，而过表达c-MYC可在一定程度上逆转这种作用。此外，MT1G过表达可降低c-MYC的表达，但增加p53的表达，表明MT1G过表达可以调节c-MYC/P53信号。研究还表明，c-MYC过表达可抑制MT1G对P53的调节作用。总之，MT1G被证实可以调节c-MYC/P53信号，抑制结直肠癌细胞的增殖、迁移和侵袭，促进其凋亡，这可能为结直肠癌的治疗提供了一种新的靶向治疗方法。 版权所有© Bentham Science Publishers；如有任何问题，请发送电子邮件至epub@benthamscience.net。

Colon cancer is a common and malignant cancer featuring high morbidity and poor prognosis.This study was performed to explore the regulatory role of MT1G in colon cancer as well as its unconcealed molecular mechanism.The expressions of MT1G, c-MYC, and p53 were assessed with the application of RT-qPCR and western blot. The impacts of MT1G overexpression on the proliferative ability of HCT116 and LoVo cells were measured by CCK-8 and BrdU incorporation assays. Additionally, transwell wound healing, and flow cytometry assays were employed to evaluate the invasive and migrative capacities as well as the apoptosis level of HCT116 and LoVo cells. Moreover, the activity of the P53 promoter region was assessed with the help of a luciferase reporter assay.It was found that the expressions of MT1G at both mRNA and protein levels were greatly decreased in human colon cancer cell lines, particularly in HCT116 and LoVo cell lines. After transfection, it was discovered that the MT1G overexpression suppressed the proliferation, migration and invasion but promoted the apoptosis of HCT116 and LoVo cells, which were then partially reversed after overexpressing c-MYC. Additionally, MT1G overexpression reduced c-MYC expression but enhanced the p53 expression, revealing that the MT1G overexpression could regulate c-MYC/P53 signal. Elsewhere, it was also shown that c-MYC overexpression suppressed the regulatory effects of MT1G on P53.To conclude, MT1G was verified to regulate c-MYC/P53 signal to repress the proliferation, migration and invasion but promote the apoptosis of colon cancer cells, which might offer a novel targeted-therapy for the improvement of colon cancer.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.