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高尔基体转运蛋白1B在人类肿瘤中的致癌作用的泛癌分析。

A pan-cancer analysis of the oncogenic role of Golgi transport 1B in human tumors.

作者信息

Tian Bo, Pang Yanan, Gao Ye, Meng Qianqian, Xin Lei, Sun Chang, Tang Xin, Wang Yilin, Li Zhaoshen, Lin Han, Wang Luowei

机构信息

Department of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai 200433, China.

Shanghai Institute of Pancreatic Diseases, Shanghai 200433, China.

出版信息

J Transl Int Med. 2023 Dec 20;11(4):433-448. doi: 10.2478/jtim-2023-0002. eCollection 2023 Dec.

DOI:10.2478/jtim-2023-0002
PMID:38130634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10732491/
Abstract

BACKGROUND

Owing to the aggressiveness and treatment-refractory nature of cancer, ideal candidates for early diagnosis and treatment are needed. Golgi transport 1B () has been associated with cellular malignant behaviors and immune responses in colorectal and lung cancer, but a systematic pan-cancer analysis on has not been conducted.

METHODS

The expression status and clinical association of in The Cancer Genome Atlas (TCGA) were analyzed. Genetic and methylation alterations in were explored. The relationship between and immune cell infiltration was also investigated. Genes related to expression were selected and analyzed.

RESULTS

was highly expressed in most tumors, and there was a positive correlation between expression and clinical pathological parameters. High expression levels of have been associated with poor prognosis of most cancers. Copy number amplification was the primary type of genetic alterations, which was related to the prognosis of pan-cancer cases. There were different levels of promoter methylation across cancer types. The methylation level of the probe cg07371838 and cg25816357 was closely associated with prognosis in diverse cancers. There was also a positive correlation between genetic alterations and CD4+ T lymphocytes, especially the Th2 subset, as well as between expression and the estimated infiltration value of cancer-associated fibroblasts. Serine/threonine kinase receptor-associated protein (), integrator complex subunit 13 (), and ethanolamine kinase 1 () were the most relevant genes for expression, and their interactions with were involved in regulating the transforming growth factor (TGF)-β receptor signaling pathway and epithelial-mesenchymal transition (EMT).

CONCLUSIONS

This pan-cancer analysis provided a comprehensive understanding of the oncogenic role of , highlighting a potential mechanism whereby influences the tumor microenvironment, as well as cancer immunotherapy.

摘要

背景

由于癌症具有侵袭性且难以治疗,因此需要寻找早期诊断和治疗的理想候选对象。高尔基体转运蛋白1B(GOLPH1B)已被证实与结直肠癌和肺癌的细胞恶性行为及免疫反应相关,但尚未对GOLPH1B进行系统的泛癌分析。

方法

分析了癌症基因组图谱(TCGA)中GOLPH1B的表达状态及其与临床的相关性。探究了GOLPH1B的基因和甲基化改变情况。还研究了GOLPH1B与免疫细胞浸润之间的关系。选择并分析了与GOLPH1B表达相关的基因。

结果

GOLPH1B在大多数肿瘤中高表达,其表达与临床病理参数呈正相关。GOLPH1B高表达与大多数癌症的不良预后相关。拷贝数扩增是GOLPH1B基因改变的主要类型,与泛癌病例的预后相关。不同癌症类型中GOLPH1B启动子甲基化水平不同。探针cg07371838和cg25816357的甲基化水平与多种癌症的预后密切相关。GOLPH1B基因改变与CD4 + T淋巴细胞,尤其是Th2亚群之间也存在正相关,GOLPH1B表达与癌症相关成纤维细胞的估计浸润值之间也呈正相关。丝氨酸/苏氨酸激酶受体相关蛋白(STRAP)、整合复合物亚基13(INTS13)和乙醇胺激酶1(EKI1)是与GOLPH1B表达最相关的基因,它们与GOLPH1B的相互作用参与调节转化生长因子(TGF)-β受体信号通路和上皮-间质转化(EMT)。

结论

这项泛癌分析全面了解了GOLPH1B的致癌作用,突出了GOLPH1B影响肿瘤微环境以及癌症免疫治疗的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/f62222c936ae/j_jtim-2023-0002_fig_008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/78e35a8db6cf/j_jtim-2023-0002_fig_001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/518ed7be47a2/j_jtim-2023-0002_fig_002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/d0388cf4d07c/j_jtim-2023-0002_fig_003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/8b81659d5321/j_jtim-2023-0002_fig_004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/b68915535d2e/j_jtim-2023-0002_fig_005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/28844a4b9935/j_jtim-2023-0002_fig_006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/354f6031f095/j_jtim-2023-0002_fig_007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/f62222c936ae/j_jtim-2023-0002_fig_008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/78e35a8db6cf/j_jtim-2023-0002_fig_001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/518ed7be47a2/j_jtim-2023-0002_fig_002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/d0388cf4d07c/j_jtim-2023-0002_fig_003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/8b81659d5321/j_jtim-2023-0002_fig_004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/b68915535d2e/j_jtim-2023-0002_fig_005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/28844a4b9935/j_jtim-2023-0002_fig_006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/354f6031f095/j_jtim-2023-0002_fig_007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def1/10732491/f62222c936ae/j_jtim-2023-0002_fig_008.jpg

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