Colorectal cancer (CRC) is the third most common tumor, with an increasing number of deaths worldwide each year. Tremendous advances in the diagnosis and treatment of CRC have significantly improved the outcomes for CRC patients. Additionally, accumulating evidence has hinted the relationship between acidic nuclear phosphoprotein 32 family member E (ANP32E) and cancer progression. But the role of ANP32E in CRC remains unclear. In our study, through TCGA database, it was demonstrated that the expression of ANP32E was enhanced in COAD tissues (n = 286). In addition, the mRNA and protein expression of ANP32E was also confirmed to be upregulated in CRC cell lines. Further investigation uncovered that knockdown of ANP32E suppressed cell proliferation and glycolysis, and facilitated cell apoptosis in CRC. Moreover, inhibition of ANP32E inhibited the AKT/mTOR pathway. Through rescue assays, we discovered that the reduced cell proliferation, glycolysis and the enhanced cell apoptosis mediated by ANP32E repression was reversed by SC79 treatment. In summary, ANP32E aggravated the growth and glycolysis of CRC cells by stimulating the AKT/mTOR pathway. This finding suggested that the ANP32E has the potential to be explored as a novel biomarker for CRC treatment.

中文翻译：

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ANP32E 的敲低通过调节 AKT/mTOR 通路抑制结直肠癌细胞生长和糖酵解

结直肠癌（CRC）是第三大常见肿瘤，全球死亡人数每年都在增加。结直肠癌诊断和治疗方面的巨大进步显着改善了结直肠癌患者的预后。此外，越来越多的证据暗示酸性核磷蛋白 32 家族成员 E (ANP32E) 与癌症进展之间的关系。但 ANP32E 在 CRC 中的作用仍不清楚。在我们的研究中，通过TCGA数据库，证明ANP32E的表达在COAD组织中增强（n= 286）。此外，ANP32E的mRNA和蛋白表达也被证实在CRC细胞系中上调。进一步的研究发现，ANP32E 的敲低可抑制细胞增殖和糖酵解，并促进结直肠癌中的细胞凋亡。此外，抑制 ANP32E 会抑制 AKT/mTOR 通路。通过挽救试验，我们发现 SC79 治疗可逆转由 ANP32E 抑制介导的细胞增殖、糖酵解减少和细胞凋亡增强。总之，ANP32E通过刺激AKT/mTOR通路加剧CRC细胞的生长和糖酵解。这一发现表明 ANP32E 有潜力被探索作为 CRC 治疗的新型生物标志物。