We aimed to explore the biological function of CPNE7 and determine the impact of CPNE7 on chemotherapy resistance in colorectal cancer (CRC) patients. According to the Gene Expression Profiling Interactive Analysis database and previously published data, CPNE7 was identified as a potential oncogene in CRC. RT‐qPCR and Western blotting were performed to verify the expression of CPNE7. Chi‐square test was used to evaluate the associations between CPNE7 and clinical features. Cell proliferation, colony formation, cell migration and invasion, cell cycle and apoptosis were assessed to determine the effects of CPNE7. Transcriptome sequencing was used to identify potential downstream regulatory genes, and gene set enrichment analysis was performed to investigate downstream pathways. The effect of CPNE7 on 5‐fluorouracil chemosensitivity was verified by half maximal inhibitory concentration (IC50). Subcutaneous tumorigenesis assay was used to examine the role of CPNE7 in sensitivity of CRC to chemotherapy in vivo. Transmission electron microscopy was used to detect autophagosomes. CPNE7 was highly expressed in CRC tissues, and its expression was correlated with T stage and tumour site. Knockdown of CPNE7 inhibited the proliferation and colony formation of CRC cells and promoted apoptosis. Knockdown of CPNE7 suppressed the expression of ATG9B and enhanced the sensitivity of CRC cells to 5‐fluorouracil in vitro and in vivo. Knockdown of CPNE7 reversed the induction of the autophagy pathway by rapamycin and reduced the number of autophagosomes. Depletion of CPNE7 attenuated the malignant proliferation of CRC cells and enhanced the chemosensitivity of CRC cells to 5‐fluorouracil.

中文翻译：

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CPNE7 的缺失通过下调 ATG9B 表达使结直肠癌对 5-氟尿嘧啶敏感

我们的目的是探索 CPNE7 的生物学功能，并确定 CPNE7 对结直肠癌 (CRC) 患者化疗耐药的影响。根据基因表达谱交互分析数据库和之前公布的数据，CPNE7被确定为结直肠癌的潜在癌基因。 RT-qPCR和Western blotting验证CPNE7的表达。使用卡方检验评估 CPNE7 与临床特征之间的关联。评估细胞增殖、集落形成、细胞迁移和侵袭、细胞周期和细胞凋亡以确定 CPNE7 的作用。使用转录组测序来识别潜在的下游调控基因，并进行基因集富集分析来研究下游通路。 CPNE7 对 5-氟尿嘧啶化疗敏感性的影响通过半数最大抑制浓度 (IC50) 进行验证。皮下肿瘤发生实验用于检测 CPNE7 在体内 CRC 对化疗敏感性中的作用。使用透射电子显微镜检测自噬体。 CPNE7在CRC组织中高表达，其表达与T分期和肿瘤部位相关。 CPNE7 的敲低抑制了 CRC 细胞的增殖和集落形成并促进细胞凋亡。 CPNE7 的敲低抑制了 ATG9B 的表达，并增强了 CRC 细胞在体外和体内对 5-氟尿嘧啶的敏感性。 CPNE7 的敲低逆转了雷帕霉素对自噬途径的诱导，并减少了自噬体的数量。 CPNE7的耗竭减弱了CRC细胞的恶性增殖并增强了CRC细胞对5-氟尿嘧啶的化学敏感性。