大肠癌（CRC）是世界上最常见和最致命的癌症之一。根据GLOBOCAN2020的全球发病率和死亡率估计，CRC是癌症的第三大主要原因，也是全球癌症相关死亡的第二大原因。美国食品药品监督管理局已批准auranofin用于治疗类风湿性关节炎。它是一种含有金的化学物质，可以抑制硫氧还蛋白还原酶。Auranofin具有多种生物活性，包括抗癌活性，尽管在CRC方面的研究不多，对CRC细胞的作用机制仍然未知。本研究的目标是观察auranofin如何影响体内和体外的CRC细胞。通过两个化学库对使CRC细胞更具响应性的药物进行了测试。使用CCK-8技术确定细胞存活率。使用穿膜试验和集落克隆实验评估细胞的侵袭、迁移和增殖情况。使用电子显微镜观察自噬体形成。还使用Western blotting确定细胞中相关蛋白的表达程度。在人SW620 CRC细胞的异种移植瘤模型中进一步测试了auranofin的抑制肿瘤作用。根据我们的发现，auranofin通过降低CRC细胞的增殖、迁移和侵袭显著减少了CRC的发生。通过mTOR依赖机制，auranofin抑制了CRC细胞的上皮间质转化（EMT）并诱导自噬作用。最后，在体内实验中显示，auranofin抑制了异种移植小鼠的肿瘤生长同时不造成损害。总之，auranofin抑制了CRC细胞的生长、侵袭和迁移。通过降低CRC细胞中EMT的发生和诱导自噬作用来抑制CRC的发生和进展，这一发现表明auranofin可能成为治疗人类CRC的潜在化疗药物。Copyright © 2023 Wolters Kluwer Health，Inc.版权所有。

Colorectal cancer (CRC) is one of the world's most common and deadly cancers. According to GLOBOCAN2020's global incidence rate and mortality estimates, CRC is the third main cause of cancer and the second leading cause of cancer-related deaths worldwide. The US Food and Drug Administration has approved auranofin for the treatment of rheumatoid arthritis. It is a gold-containing chemical that inhibits thioredoxin reductase. Auranofin has a number of biological activities, including anticancer activity, although it has not been researched extensively in CRC, and the mechanism of action on CRC cells is still unknown. The goal of this research was to see how Auranofin affected CRC cells in vivo and in vitro. The two chemical libraries were tested for drugs that make CRC cells more responsive. The CCK-8 technique was used to determine the cell survival rate. The invasion, migration, and proliferation of cells were assessed using a transwell test and a colony cloning experiment. An electron microscope was used to observe autophagosome formation. Western blotting was also used to determine the degree of expression of related proteins in cells. Auranofin's tumor-suppressing properties were further tested in a xenograft tumor model of human SW620 CRC cells. Auranofin dramatically reduced the occurrence of CRC by decreasing the proliferation, migration, and invasion of CRC cells, according to our findings. Through a mTOR-dependent mechanism, auranofin inhibits the epithelial-mesenchymal transition (EMT) and induces autophagy in CRC cells. Finally, in-vivo tests revealed that auranofin suppressed tumor growth in xenograft mice while causing no harm. In summary, auranofin suppresses CRC cell growth, invasion, and migration. Auranofin inhibits the occurrence and progression of CRC by decreasing EMT and inducing autophagy in CRC cells via a mTOR-dependent mechanism. These findings suggest that auranofin could be a potential chemotherapeutic medication for the treatment of human CRC.Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.