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POM121 是一种预测喉癌预后的新型标志物。

POM121 is a novel marker for predicting the prognosis of laryngeal cancer.

机构信息

Emergency Center, Bayannur Hospital, Bayannur, China.

Department of Stomatology, Children's Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Histol Histopathol. 2020 Nov;35(11):1285-1293. doi: 10.14670/HH-18-267. Epub 2020 Oct 5.

DOI:10.14670/HH-18-267
PMID:33016327
Abstract

The nuclear pore membrane protein 121 (POM121) is an important member of the nuclear pore complex which regulates nucleocytoplasmic transport, but little is known about the role of POM121 in laryngeal cancer. In this study, quantitative real-time polymerase chain reaction and immunohistochemistry were performed to detect POM121 expression in laryngeal tissues. The associations between POM121 and clinicopathological characteristics and overall survival in laryngocarcinoma patients were also analyzed. The mechanism of POM121 was preliminarily explored through gene set enrichment analysis (GSEA). mRNA and protein expression of POM121 in laryngocarcinoma tissues were higher than those in nontumor tissues. High POM121 expression was positively correlated with poor differentiation (χ²=42.391, P<0.001), advanced distant metastases (χ²=20.346, P<0.001) and TNM stage (χ²=23.436, P<0.001). Laryngocarcinoma patients with high POM121 level tended to have poor overall survival. GSEA confirmed that the mechanism of POM121 in laryngeal cancer may relate to sphingolipid metabolism, lysosome, fatty acid metabolism, ribosome, nucleotide excision repair and the PPAR signaling pathway. Overall, POM121 expression might be a prognostic biomarker in laryngeal cancer, and POM121 has the potential to present as a therapeutic target for laryngocarcinoma patients.

摘要

核孔膜蛋白 121(POM121)是核孔复合物的重要成员,调节核质转运,但关于 POM121 在喉癌中的作用知之甚少。本研究通过实时定量聚合酶链反应和免疫组织化学检测了喉组织中 POM121 的表达。还分析了 POM121 与喉癌患者临床病理特征和总生存的关系。通过基因集富集分析(GSEA)初步探讨了 POM121 的作用机制。喉癌组织中 POM121 的 mRNA 和蛋白表达均高于非肿瘤组织。高 POM121 表达与低分化(χ²=42.391,P<0.001)、晚期远处转移(χ²=20.346,P<0.001)和 TNM 分期(χ²=23.436,P<0.001)呈正相关。POM121 水平高的喉癌患者总生存较差。GSEA 证实 POM121 在喉癌中的作用机制可能与鞘脂代谢、溶酶体、脂肪酸代谢、核糖体、核苷酸切除修复和 PPAR 信号通路有关。总之,POM121 的表达可能是喉癌的预后生物标志物,POM121 有可能成为喉癌患者的治疗靶点。

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本文引用的文献

1
POM121 overexpression is related to a poor prognosis in colorectal cancer.POM121 过表达与结直肠癌的不良预后相关。
Expert Rev Mol Diagn. 2020 Mar;20(3):345-353. doi: 10.1080/14737159.2020.1707670. Epub 2019 Dec 24.
2
POM121 is identified as a novel prognostic marker of oral squamous cell carcinoma.POM121被鉴定为口腔鳞状细胞癌的一种新型预后标志物。
J Cancer. 2019 Jul 24;10(19):4473-4480. doi: 10.7150/jca.33368. eCollection 2019.
3
POM121 inhibits the macrophage inflammatory response by impacting NF-κB P65 nuclear accumulation.
治疗性靶向核输出和进口受体在癌症及其在联合化疗中的潜力。
IUBMB Life. 2024 Jan;76(1):4-25. doi: 10.1002/iub.2773. Epub 2023 Aug 25.
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Integrative analysis of circadian clock with prognostic and immunological biomarker identification in ovarian cancer.卵巢癌中昼夜节律钟与预后及免疫生物标志物识别的综合分析
Front Mol Biosci. 2023 Jun 20;10:1208132. doi: 10.3389/fmolb.2023.1208132. eCollection 2023.
5
POM121 promotes the proliferation and metastasis of gastric cancer via PI3K/AKT/MYC pathway.POM121通过PI3K/AKT/MYC信号通路促进胃癌的增殖和转移。
Am J Cancer Res. 2023 Feb 15;13(2):485-497. eCollection 2023.
6
CircINTS4 Facilitates Chemoresistance of TNBC by Competitively Binding miR-129-5p/POM121 Axis.环状INTS4通过竞争性结合miR-129-5p/POM121轴促进三阴性乳腺癌的化疗耐药性。
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In Pursuit of Distinctiveness: Transmembrane Nucleoporins and Their Disease Associations.追求独特性:跨膜核孔蛋白及其与疾病的关联
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POM121 通过影响 NF-κB P65 核积累抑制巨噬细胞炎症反应。
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Expression and role of EGFR, cyclin D1 and KRAS in laryngocarcinoma tissues.表皮生长因子受体(EGFR)、细胞周期蛋白D1(cyclin D1)及KRAS在喉癌组织中的表达及作用
Exp Ther Med. 2019 Jan;17(1):782-790. doi: 10.3892/etm.2018.7027. Epub 2018 Nov 28.
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Targeting Nucleoporin POM121-Importin β Axis in Prostate Cancer.靶向前列腺癌中的核孔蛋白 POM121-Importin β 轴。
Cell Chem Biol. 2018 Sep 20;25(9):1056-1058. doi: 10.1016/j.chembiol.2018.09.003.
6
Nuclear Pores Promote Lethal Prostate Cancer by Increasing POM121-Driven E2F1, MYC, and AR Nuclear Import.核孔通过增加 POM121 驱动的 E2F1、MYC 和 AR 核输入促进致命性前列腺癌。
Cell. 2018 Aug 23;174(5):1200-1215.e20. doi: 10.1016/j.cell.2018.07.015. Epub 2018 Aug 9.
7
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