目的：研究胰岛素样生长因子2 mRNA结合蛋白2（IGF2BP2）对结直肠癌细胞增殖、迁移和肿瘤免疫微环境的影响及其可能的分子机制。方法：使用癌症基因组图谱（TCGA）数据库分析结直肠癌和相邻组织中IGF2BP2和MYC的表达水平。通过RNA干扰（RNAi）静默HCT-116和SW480人结直肠癌细胞中的IGF2BP2，并通过定量实时PCR检测沉默效果。静默IGF2BP2后，采用集落形成实验、CCK-8实验和5-乙炔基-2'-脱氧尿嘧啶（EdU）实验来检测细胞集落形成和增殖能力。使用TranswellTM实验检测细胞迁移能力。采用定量实时PCR检测IGF2BP2，MYC，肿瘤坏死因子-α（TNF-α），转化生长因子-β（TGF-β）和白细胞介素-10（IL-10） mRNA表达。通过Western blot检测IGF2BP2和MYC的蛋白表达。通过RNA免疫共沉淀后采用定量实时PCR检测IGF2BP2和MYC在HCT-116细胞中的结合能力。结果：TCGA数据库的结果显示，结直肠癌组织中IGF2BP2和MYC的表达显著高于相邻组织，并且IGF2BP2高表达的结直肠癌患者生存时间较短。静默IGF2BP2后，HCT-116和SW480细胞的活力、增殖和迁移能力显著降低。IGF2BP2敲低组中MYC、TGF-β和IL-10 mRNA的表达显著下调，而TNF-α mRNA的表达增加。MYC蛋白表达和MYC mRNA的稳定性显著下调。RIP-qPCR的结果显示，IGF2BP2可以结合MYC mRNA。结论：静默IGF2BP2通过下调MYC的表达来抑制结直肠癌细胞增殖、迁移并促进肿瘤免疫。

Objective To investigate the effect of insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) on the proliferation, migration and tumor immune microenvironment of colorectal cancer cells and its possible molecular mechanism. Methods The Cancer Genome Atlas (TCGA) database was used to analyze the expression levels of IGF2BP2 and MYC in colorectal cancer and adjacent tissues. The expression of IGF2BP2 in HCT-116 and SW480 human colorectal cancer cells was silenced by RNA interference (RNAi), and the silencing effect was detected by quantitative real-time PCR. After knocking down IGF2BP2, colony formation assay, CCK-8 assay and 5-ethynyl-2'-deoxyuridine (EdU) assay were employed to detect cell colony formation and proliferation ability. TranswellTM assay was used to detect cell migration ability. Quantitative real-time PCR was used to detect the mRNA expression of IGF2BP2, MYC, tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β) and interleukin-10 (IL-10). The protein expression of IGF2BP2 and MYC was detected by western blot. The binding ability of IGF2BP2 and MYC in HCT-116 cells was detected by quantitative real-time PCR after RNA immunoprecipitation. Results The results of TCGA database showed that the expression of IGF2BP2 and MYC in colorectal cancer tissues was significantly higher than that in adjacent tissues, and the survival time of colorectal cancer patients with high expression of IGF2BP2 was shorter. After silencing IGF2BP2, the viability, proliferation and migration of HCT-116 and SW480 cells were decreased. The mRNA expression of MYC, TGF-β and IL-10 in IGF2BP2 knockdown group was significantly decreased, while the expression of TNF-α mRNA was increased. The expression of MYC protein and the stability of MYC mRNA were significantly decreased. RIP-qPCR results showed that IGF2BP2 could bind to MYC mRNA. Conclusion Knockdown of IGF2BP2 inhibits colorectal cancer cell proliferation, migration and promotes tumor immunity by down-regulating MYC expression.