在结直肠癌（CRC）的发生和发展中，网络调节的分子机制不断得到改进。在这里，我们研究了TEAD4-MAD2L1轴对人类CRC细胞增殖和转移的生物学影响。这项研究揭示了CRC组织和CRC细胞系中MAD2L1和TEAD4的表达显著高于相邻的上皮组织和正常肠上皮细胞系NCM460，它们的表达显著呈正相关；此外，抑制MAD2L1或TEAD4的表达可抑制CRC细胞的增殖和迁移，并促进凋亡。此外，MAD2L1基因的启动子区域具有TEAD4结合位点（基序序列），并且MAD2L1的转录受到TEAD4蛋白的正向调节；通过沉默TEAD4可以抑制CRC细胞的促进/迁移和促进凋亡，但高表达MAD2L1可以挽救这种影响。总之，我们的研究表明，MAD2L1的转录和表达受TEAD4的调节，进一步促进了体外和体内CRC细胞的增殖和迁移，抑制了凋亡。MAD2L1和TEAD4是结直肠癌的潜在生物标志物。©2022年。作者，独家许可给Springer Nature America, Inc.

The molecular mechanism of network regulation in the occurrence and development of colorectal cancer (CRC) has been constantly improved. Here, we investigated the biological effects of TEAD4-MAD2L1 axis on proliferation and metastasis of human CRC cells. This study revealed that the expressions of MAD2L1 and TEAD4 in CRC tissues and CRC cell lines were significantly higher than those in adjacent epithelial tissues and normal intestinal epithelial cell line NCM460, and their expressions were significantly positively correlated; Moreover, inhibiting the expression of MAD2L1 or TEAD4 can inhibit the proliferation and migration of CRC cells and promote apoptosis. In addition, the promoter region of MAD2L1 gene has a TEAD4 binding site (motif sequence), and the transcription of MAD2L1 is positively regulated by TEAD4 protein; The inhibition of promotion/migration and promotion of apoptosis of CRC cells by silencing TEAD4 can be saved by the high expression of MAD2L1. In conclusion, our study suggests that the transcription and expression of MAD2L1 is regulated by TEAD4, which further promotes the proliferation and migration of CRC cells in vitro and in vivo, and inhibits apoptosis. MAD2L1 and TEAD4 are potential biomarkers for colorectal cancer.© 2022. The Author(s), under exclusive licence to Springer Nature America, Inc.