Colorectal cancer (CRC) is a worldwide health concern. Chronic inflammation is a risk factor for CRC, and interleukin-6 (IL-6) plays a pivotal role in this process. Arginine-specific mono-ADP-ribosyltransferase-1 (ART1) positively regulates inflammatory cytokines. ART1 knockdown reduces the level of glycoprotein 130 (gp130), a key transducer in the IL-6 signalling pathway. However, the relationship between ART1 and IL-6 and the resulting effects on IL-6-induced proliferation in CRC cells remain unclear. The aims of this study were to investigate the effects of ART1 knockdown on IL-6-induced cell proliferation in vitro and use an in vivo murine model to observe the growth of transplanted tumours. The results showed that compared with the control, ART1-sh cancer cells induced by IL-6 exhibited reduced viability, a lower rate of colony formation, less DNA synthesis, decreased protein levels of gp130, c-Myc, cyclin D1, Bcl-xL, and a reduced p-STAT3/STAT3 ratio (P < 0.05). Moreover, mice transplanted with ART1-sh CT26 cells that had high levels of IL-6 displayed tumours with smaller volumes (P < 0.05). ART1 and gp130 were colocalized in CT26, LoVo and HCT116 cells, and their expression was positively correlated in human CRC tissues. Overall, ART1 may serve as a promising regulatory factor for IL-6 signalling and a potential therapeutic target for human CRC.

中文翻译：

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ART1敲低可降低IL-6诱导的结直肠癌细胞增殖

结直肠癌（CRC）是一个全球性的健康问题。慢性炎症是结直肠癌的危险因素，白细胞介素6 (IL-6) 在此过程中发挥着关键作用。精氨酸特异性单 ADP 核糖基转移酶 1 (ART1) 正向调节炎症细胞因子。ART1 敲低会降低糖蛋白 130 (gp130) 的水平，糖蛋白 130 是 IL-6 信号通路中的关键转导因子。然而，ART1 和 IL-6 之间的关系以及由此产生的对 IL-6 诱导的 CRC 细胞增殖的影响仍不清楚。本研究的目的是在体外研究 ART1 敲低对 IL-6 诱导的细胞增殖的影响，并使用体内小鼠模型观察移植肿瘤的生长。结果显示，与对照相比，IL-6诱导的ART1-sh癌细胞活力降低，集落形成率降低，DNA合成减少，gp130、c-Myc、cyclin D1、Bcl-xL蛋白水平降低，以及 p-STAT3/STAT3 比率降低 (P < 0.05)。此外，移植IL-6水平高的ART1-sh CT26细胞的小鼠显示肿瘤体积更小（P < 0.05）。ART1和gp130共定位于CT26、LoVo和HCT116细胞中，并且它们的表达在人结直肠癌组织中呈正相关。总的来说，ART1可能作为IL-6信号传导的一个有前途的调节因子和人类结直肠癌的潜在治疗靶点。