Tazarotene-induced gene 1 (TIG1) is considered to be a tumor suppressor gene that is highly expressed in normal or well-differentiated colon tissues, while downregulation of TIG1 expression occurs in poorly differentiated colorectal cancer (CRC) tissues. However, it is still unclear how TIG1 regulates the tumorigenesis of CRC. Polo-like kinases (Plks) are believed to play an important role in regulating the cell cycle. The performance of PLK2 in CRC is negatively correlated with the differentiation status of CRC tissues. Here, we found that PLK2 can induce the growth of CRC cells and that TIG1 can prevent PLK2 from promoting the proliferation of CRC cells. We also found that the expression of PLK2 in CRC cells was associated with low levels of Fbxw7 protein and increased expression of cyclin E1. When TIG1 was coexpressed with PLK2, the changes in Fbxw7/cyclin E1 levels induced by PLK2 were reversed. In contrast, silencing TIG1 promoted the proliferation of CRC, and when PLK2 was also silenced, the proliferation of CRC cells induced by TIG1 silencing was significantly inhibited. The above research results suggest that TIG1 can regulate the tumorigenesis of CRC by regulating the activity of PLK2.

中文翻译：

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他扎罗汀诱导的基因 1 与 Polo 样激酶 2 相互作用并抑制 HCT116 结直肠癌细胞中的细胞增殖


他扎罗汀诱导基因1（TIG1）被认为是一种抑癌基因，在正常或分化良好的结肠组织中高表达，而在低分化结直肠癌（CRC）组织中TIG1表达下调。然而，目前尚不清楚TIG1如何调控CRC的肿瘤发生。 Polo 样激酶 (Plk) 被认为在调节细胞周期中发挥重要作用。 PLK2在CRC中的表现与CRC组织的分化状态呈负相关。在这里，我们发现PLK2可以诱导CRC细胞的生长，而TIG1可以阻止PLK2促进CRC细胞的增殖。我们还发现CRC细胞中PLK2的表达与Fbxw7蛋白的低水平和cyclin E1的表达增加有关。当TIG1与PLK2共表达时，PLK2诱导的Fbxw7/cyclin E1水平的变化被逆转。相反，沉默TIG1促进了CRC的增殖，并且当PLK2也被沉默时，TIG1沉默诱导的CRC细胞的增殖被显着抑制。上述研究结果提示TIG1可以通过调节PLK2的活性来调控CRC的肿瘤发生。