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肌动蛋白相关蛋白2/3复合体亚基1B通过调节AKT/PI3K/mTOR信号通路促进卵巢癌进展。

Actin-related protein 2/3 complex subunit 1B promotes ovarian cancer progression by regulating the AKT/PI3K/mTOR signaling pathway.

作者信息

Ke Miao, Zhu Huimin, Lin Yu, Zhang Ying, Tang Tao, Xie Yuhao, Chen Zhe-Sheng, Wang Xiaoyu, Shen Yuan

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan University, Guangzhou 510630, Guangdong Province, China.

Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzho 510630, Guangdong Province, China.

出版信息

J Transl Int Med. 2024 Oct 1;12(4):406-423. doi: 10.2478/jtim-2024-0025. eCollection 2024 Sep.

DOI:10.2478/jtim-2024-0025
PMID:39360160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11444474/
Abstract

BACKGROUND AND OBJECTIVES

Actin-related protein 2/3 complex subunit 1B (ARPC1B) is an essential subunit of the actin-related protein 2/3 (Arp2/3) complex. While there have been numerous research reports on Arp2/3 in relation to tumors, there needs to be more research on ARPC1B and its role in tumors, particularly at the pan-cancer level.

METHODS

Utilizing data from the cancer genome atlas (TCGA) and genotype-tissue expression (GTEx) databases, we analyzed ARPC1B expression differences in normal, tumor, and adjacent tissues, investigating its correlation with prognosis and clinical stages in various cancers. We conducted gene enrichment analysis and explored ARPC1B's connection to the tumor immune microenvironment and its impact on anti-tumor drug resistance. In addition, and experiments have also been carried out to find the mechanism of ARPC1B on ovarian cancer (OV) proliferation and invasion.

RESULTS

ARPC1B was highly expressed in 33 tumor types, suggesting its role as a tumor-promoting factor. Its expression correlated with poor prognosis and served as a clinical staging marker in over 10 tumor types. ARPC1B is implicated in various biological processes and signaling pathways, uniquely associated with tumor immunity, indicating immunosuppressive conditions in high-expression cases. High ARPC1B expression was linked to resistance to six anti-tumor drugs. Further experiments showed that ARPC1B can affect the proliferation, apoptosis, migration, and invasion of OV cells through the AKT/PI3K/mTOR pathway.

CONCLUSION

ARPC1B is a biomarker for immune suppression, prognosis, clinical staging, and drug resistance, providing new insights for cancer therapeutics.

摘要

背景与目的

肌动蛋白相关蛋白2/3复合体亚基1B(ARPC1B)是肌动蛋白相关蛋白2/3(Arp2/3)复合体的一个必需亚基。虽然已有众多关于Arp2/3与肿瘤相关的研究报道,但对于ARPC1B及其在肿瘤中的作用,尤其是在泛癌水平上,仍需更多研究。

方法

利用癌症基因组图谱(TCGA)和基因型-组织表达(GTEx)数据库的数据,我们分析了ARPC1B在正常组织、肿瘤组织和癌旁组织中的表达差异,研究其与多种癌症的预后和临床分期的相关性。我们进行了基因富集分析,并探讨了ARPC1B与肿瘤免疫微环境的联系及其对抗肿瘤耐药性的影响。此外,还开展了实验以探究ARPC1B对卵巢癌(OV)增殖和侵袭的作用机制。

结果

ARPC1B在33种肿瘤类型中高表达,表明其作为肿瘤促进因子的作用。其表达与不良预后相关,并在10多种肿瘤类型中作为临床分期标志物。ARPC1B参与多种生物学过程和信号通路,与肿瘤免疫独特相关,表明高表达情况下存在免疫抑制状态。ARPC1B高表达与六种抗肿瘤药物耐药相关。进一步实验表明,ARPC1B可通过AKT/PI3K/mTOR途径影响OV细胞的增殖、凋亡、迁移和侵袭。

结论

ARPC1B是免疫抑制、预后、临床分期和耐药性的生物标志物,为癌症治疗提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/300857091319/j_jtim-2024-0025_fig_008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/0f5f22168485/j_jtim-2024-0025_fig_001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/53e7efa95135/j_jtim-2024-0025_fig_002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/77efca042660/j_jtim-2024-0025_fig_003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/e2614664d762/j_jtim-2024-0025_fig_004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/4dc199176da5/j_jtim-2024-0025_fig_005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/44eb652d9d54/j_jtim-2024-0025_fig_006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/a9cb5d49de57/j_jtim-2024-0025_fig_007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/300857091319/j_jtim-2024-0025_fig_008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/0f5f22168485/j_jtim-2024-0025_fig_001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/53e7efa95135/j_jtim-2024-0025_fig_002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/77efca042660/j_jtim-2024-0025_fig_003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/e2614664d762/j_jtim-2024-0025_fig_004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/4dc199176da5/j_jtim-2024-0025_fig_005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/44eb652d9d54/j_jtim-2024-0025_fig_006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/a9cb5d49de57/j_jtim-2024-0025_fig_007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b638/11444474/300857091319/j_jtim-2024-0025_fig_008.jpg

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