大肠癌（CRC）是一种影响消化系统的恶性肿瘤。随着社会现代化的增加，全球的大肠癌发病率也在增加。ELK1作为一种转录因子，在大肠癌中得到广泛研究。然而，关于ELK1具体作用机制仍存在许多未知因素。本研究探讨了ELK1及其下游通路在CRC发生发展中的作用。基于临床样本，本研究检测了CRC细胞中miR-31-5p的表达，并研究其对恶性行为（迁移、侵袭、凋亡）和自噬的影响。miR-31-5p的启动子序列从UCSC数据库获得，并鉴定ELK1为其转录因子。在ELK1敲除的CRC细胞中，miR-31-5p得到过表达，并分析了其对恶性行为和自噬的影响。通过双荧光素酶检测法预测和验证了CDIP1作为miR-31-5p的靶基因。评估了CDIP1在CRC细胞的恶性行为中的影响，并使用CDIP1 siRNA作为对miR-31-5p抑制的救治。通过体内实验证实了ELK1/miR-31-5p在肿瘤生长中的作用。miR-31-5p的表达在大肠癌组织和细胞中上调。miR-31-5p的敲除显著抑制了癌细胞的恶性行为并介导了自噬。确认ELK1与miR-31-5p启动子结合并增强其转录。发现miR-31-5p与CDIP1 3'UTR结合并抑制CDIP1的表达。CDIP1 siRNA部分恢复了miR-31-5p敲除对细胞转移能力、自噬和凋亡的影响。基于体内实验结果，显示ELK1/miR-31-5p轴在裸鼠中正调控肿瘤生长。我们的研究结果表明ELK1通过miR-31-5p/CDIP1轴调控大肠癌的进展，并且ELK1/miR-31-5p/CDIP1轴可能成为大肠癌的治疗靶点。©2023 Yan and Lei.

Colorectal cancer (CRC) is a malignant tumor that affects the digestive system. With the increased of modernization of society, the incidence of colorectal cancer has increased throughout the world. As a transcription factor, ELK1 has been widely studied in colorectal cancer. However, there are still many unknown factors regarding its specific mechanism of action.This study explored the role of ELK1 and its downstream pathway in CRC pathogenesis.Based on clinical samples, this study examined miR-31-5p expression in CRC cells and its impact on malignant behaviors (migration, invasion, apoptosis) and autophagy. The promoter sequence of miR-31-5p was obtained from the UCSC database, and ELK1 was identified as its transcription factor. In ELK1-knockdown CRC cells, miR-31-5p was overexpressed, and its response in malignant behaviors and autophagy was analyzed. The target gene CDIP1 was predicted and verified using a dual-luciferase assay. The influence of CDIP1 on malignant behavior in CRC cells was assessed, and CDIP1 siRNA was used as a rescue treatment for miR-31-5p inhibition. The role of ELK1/miR-31-5p in tumor growth was validated in vivo.miR-31-5p expression was upregulated in the colorectal cancer tissues and cells. The knockdown of miR-31-5p markedly inhibited cancer cells' malignant behaviors and mediated autophagy. ELK1 was confirmed to bind with the miR-31-5p promoter and enhance miR-31-5p transcription. miR-31-5p was found to bind with the CDIP1 3'UTR and inhibit CDIP1 expression. CDIP1 siRNA partially rescued the effects of miR-31-5p knockdown on cell metastatic ability, autophagy, and apoptosis. Based on the in vivo experiments, results showed that the ELK1/miR-31-5p axis positively regulated tumor growth in nude mice.Our findings indicate that ELK1 regulates the progression of colorectal cancer via an miR-31-5p/CDIP1 axis, and the ELK1/miR-31-5p/CDIP1 axis could be a therapeutic target for colorectal cancer.©2023 Yan and Lei.