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敲低ANP32E通过调节AKT/mTOR途径抑制结肠癌细胞的生长和糖酵解。

Knockdown of ANP32E inhibits colorectal cancer cell growth and glycolysis by regulating the AKT/mTOR pathway.

作者信息

Liu Jiaojiao, Liu Yanchao, Zhao Qi

机构信息

Department of Clinical Laboratory, Beihua University Affiliated Hospital, No. 12, Jiefang Middle Road, Jilin, Jilin, 132011, China.

Department of Clinical Laboratory, Jilin Gynecology and Obstetrics Hospital, Jilin, Jilin, 130211, China.

出版信息

Open Life Sci. 2024 Mar 9;19(1):20220817. doi: 10.1515/biol-2022-0817. eCollection 2024.

DOI:10.1515/biol-2022-0817
PMID:38585643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10997116/
Abstract

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 ( = 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.

摘要

结直肠癌(CRC)是第三大常见肿瘤,全球每年的死亡人数呈上升趋势。CRC诊断和治疗方面的巨大进展显著改善了CRC患者的治疗效果。此外,越来越多的证据暗示了酸性核磷蛋白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数据库表明,ANP32E在结肠癌组织(n = 286)中的表达增强。此外,还证实ANP32E在CRC细胞系中的mRNA和蛋白表达上调。进一步研究发现,敲低ANP32E可抑制CRC细胞增殖和糖酵解,并促进细胞凋亡。此外,抑制ANP32E可抑制AKT/mTOR通路。通过拯救实验,我们发现SC79处理可逆转由ANP32E抑制介导的细胞增殖减少、糖酵解减少和细胞凋亡增加。总之,ANP32E通过刺激AKT/mTOR通路加重了CRC细胞的生长和糖酵解。这一发现表明,ANP32E有潜力作为CRC治疗的新型生物标志物进行探索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/5446ba5bf24b/j_biol-2022-0817-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/8b13d4e87e05/j_biol-2022-0817-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/2babfa9d6292/j_biol-2022-0817-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/22fcc5357172/j_biol-2022-0817-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/fc7435eb4d1e/j_biol-2022-0817-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/5446ba5bf24b/j_biol-2022-0817-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/8b13d4e87e05/j_biol-2022-0817-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/2babfa9d6292/j_biol-2022-0817-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/22fcc5357172/j_biol-2022-0817-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/fc7435eb4d1e/j_biol-2022-0817-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb84/10997116/5446ba5bf24b/j_biol-2022-0817-fig005.jpg

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