Colorectal cancer (CRC) is one of the most often diagnosed cancers globally. MicroRNAs are small RNA molecules that play essential roles in tumorigenesis and progression of CRC. Here we evaluated the effects of miR-141-3p on growth, cetuximab sensitivity, migration and invasion of CRC cells. We found that miR-141-3p negatively regulated the proliferation, migration and invasion in CRC cells. In addition, miR-141-3p enhanced the cetuximab sensitivity of CRC cells by EGFR suppression. Moreover, miR-141-3p improved cetuximab-induced apoptosis in CRC cells. Furthermore, miR-141-3p altered the expression of E-cadherin, N-cadherin, snail and Vimentin, indicating miR-141-3p might play a role on epithelial to mesenchymal transition (EMT). Luciferase reporter assay showed that EGFR was the direct binding site of miR-141-3p and the expression levels of p-EGFR, Raf-1, pAKT and p-ERK1/2 were regulated by miR-141-3p. After down-regulation of EGFR by siRNA in CRC cells, the effects of miR-141-3p on proliferation, migration and invasion were reversed. miR-141-3p played important roles in CRC growth and response to cetuximab treatment, and might function as a potential biomarker to predict cetuximab response.

大肠癌（CRC）是全球最常被诊断的癌症之一。微小RNA是在CRC的发生和发展中起重要作用的小RNA分子。在这里，我们评估了miR-141-3p对CRC细胞生长，西妥昔单抗敏感性，迁移和侵袭的影响。我们发现，miR-141-3p负调控CRC细胞的增殖，迁移和侵袭。此外，miR-141-3p通过EGFR抑制作用增强了CRC细胞的西妥昔单抗敏感性。此外，miR-141-3p改善了西妥昔单抗诱导的CRC细胞凋亡。此外，miR-141-3p改变了E-cadherin，N-cadherin，snail和Vimentin的表达，表明miR-141-3p可能在上皮到间质转化（EMT）中起作用。萤光素酶报告基因检测表明，EGFR是miR-141-3p的直接结合位点，miR-141-3p调节p-EGFR，Raf-1，pAKT和p-ERK1 / 2的表达水平。siRNA下调CRC细胞中EGFR的表达后，miR-141-3p对增殖，迁移和侵袭的作用被逆转。miR-141-3p在CRC的生长和对西妥昔单抗治疗的反应中起重要作用，并且可能充当预测西妥昔单抗反应的潜在生物标志物。