Microchromosome maintenance protein 7 (MCM7), a DNA replication permitting factor, plays an essential role in initiating DNA replication. MCM7 is reported to be involved in tumor formation and progression, whereas the expression profile and molecular function of MCM7 in colorectal cancer (CRC) remain unknown. In this study, we aimed to evaluate the clinical significance and biological function of MCM7 in CRC and investigated whether MCM7 can be used for a differential diagnosis in CRC and whether it may serve as a more sensitive proliferation marker for CRC evaluation. Moreover, immunohistochemical analysis of MCM7 was performed in a total of 89 specimens, and high MCM7 expression levels were associated with worse overall survival (OS) in CRC patients. Furthermore, the cell functional test suggested that lentivirus-mediated silencing of MCM7 with shRNA in CRC cells significantly inhibited cellular proliferation and promoted apoptosis in vitro and inhibited tumor growth in vivo. Additionally, mechanistic studies further demonstrated that P21-activated protein kinase 2 (PAK2) was regulated by MCM7 via microarray analysis and cell functional recovery tests, and miR-107 played a role in regulating expression MCM7 via miRNA microarray analysis and 3’UTR reporter assays. Taken together, our results suggest that the miR-107/MCM7/PAK2 pathway may participate in cancer progression and that MCM7 may serve as a prognostic biomarker in CRC

微染色体维持蛋白 7 (MCM7) 是一种 DNA 复制允许因子，在启动 DNA 复制中起重要作用。据报道 MCM7 参与肿瘤的形成和进展，而 MCM7 在结直肠癌 (CRC) 中的表达谱和分子功能仍然未知。在本研究中，我们旨在评估 MCM7 在 CRC 中的临床意义和生物学功能，并研究 MCM7 是否可用于 CRC 的鉴别诊断以及它是否可作为更敏感的 CRC 评估增殖标志物。此外，对总共 89 个样本进行了 MCM7 的免疫组织化学分析，高 MCM7 表达水平与 CRC 患者较差的总生存期 (OS) 相关。此外，细胞功能测试表明慢病毒介导的MCM7与shRNA在CRC细胞中的沉默在体外显着抑制细胞增殖并促进细胞凋亡并抑制体内肿瘤生长。此外，机制研究进一步表明 P21 活化蛋白激酶 2 (PAK2) 通过微阵列分析和细胞功能恢复测试受 MCM7 调节，并且 miR-107 通过 miRNA 微阵列分析和 3'UTR 报告基因检测在调节 MCM7 表达中发挥作用. 总之，我们的结果表明 miR-107/MCM7/PAK2 通路可能参与癌症进展，并且 MCM7 可能作为 CRC 的预后生物标志物 机制研究进一步表明 P21 活化蛋白激酶 2 (PAK2) 通过微阵列分析和细胞功能恢复测试受 MCM7 调节，并且 miR-107 通过 miRNA 微阵列分析和 3'UTR 报告基因测定在调节 MCM7 表达中发挥作用。总之，我们的结果表明 miR-107/MCM7/PAK2 通路可能参与癌症进展，并且 MCM7 可能作为 CRC 的预后生物标志物 机制研究进一步表明 P21 活化蛋白激酶 2 (PAK2) 通过微阵列分析和细胞功能恢复测试受 MCM7 调节，并且 miR-107 通过 miRNA 微阵列分析和 3'UTR 报告基因测定在调节 MCM7 表达中发挥作用。总之，我们的结果表明 miR-107/MCM7/PAK2 通路可能参与癌症进展，并且 MCM7 可能作为 CRC 的预后生物标志物