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关于癌蛋白乙型肝炎病毒 X 相互作用蛋白的研究进展(综述)。

Research progress on oncoprotein hepatitis B X‑interacting protein (Review).

机构信息

Chronic Disease Research Center, Medical College, Dalian University, Dalian, Liaoning 116622, P.R. China.

Chronic Disease Research Center, Medical College, Dalian University, Dalian, Liaoning 116622, P.R. China.

出版信息

Mol Med Rep. 2024 Jun;29(6). doi: 10.3892/mmr.2024.13213. Epub 2024 Apr 5.

DOI:10.3892/mmr.2024.13213
PMID:38577934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11019400/
Abstract

Hepatitis B X‑interacting protein (HBXIP) is a membrane protein located on the lysosomal surface and encoded by the Lamtor gene. It is expressed by a wide range of tumor types, including breast cancer, esophageal squamous cell carcinoma and hepatocellular carcinoma, and its expression is associated with certain clinicopathological characteristics. In the past decade, research on the oncogenic mechanisms of HBXIP has increased and the function of HBXIP in normal cells has been gradually elucidated. In the present review, the following was discussed: The normal physiological role of the HBXIP carcinogenic mechanism; the clinical significance of high levels of HBXIP expression in different tumors; HBXIP regulation of transcription, post‑transcription and post‑translation processes in tumors; the role of HBXIP in improving the antioxidant capacity of tumor cells; the inhibition of ferroptosis of tumor cells and regulating the metabolic reprogramming of tumor cells; and the role of HBXIP in promoting the malignant progression of tumors. In conclusion, the present review summarized the existing knowledge of HBXIP, established its carcinogenic mechanism and discussed future related research on HBXIP.

摘要

乙型肝炎病毒 X 相互作用蛋白 (HBXIP) 是一种位于溶酶体表面的膜蛋白,由 Lamtor 基因编码。它在多种肿瘤类型中表达,包括乳腺癌、食管鳞状细胞癌和肝细胞癌,其表达与某些临床病理特征相关。在过去的十年中,对 HBXIP 致癌机制的研究增加了,并且 HBXIP 在正常细胞中的功能也逐渐阐明。在本综述中,讨论了以下内容:HBXIP 致癌机制的正常生理作用;不同肿瘤中 HBXIP 高表达的临床意义;HBXIP 在肿瘤中转录、转录后和翻译后过程中的调节作用;HBXIP 提高肿瘤细胞抗氧化能力的作用;抑制肿瘤细胞铁死亡和调节肿瘤细胞代谢重编程的作用;以及 HBXIP 在促进肿瘤恶性进展中的作用。总之,本综述总结了目前对 HBXIP 的认识,建立了其致癌机制,并讨论了未来关于 HBXIP 的相关研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/fcc4358314f7/mmr-29-06-13213-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/68293112f5a1/mmr-29-06-13213-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/640bed5b84f5/mmr-29-06-13213-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/fcc4358314f7/mmr-29-06-13213-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/68293112f5a1/mmr-29-06-13213-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/640bed5b84f5/mmr-29-06-13213-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07ee/11019400/fcc4358314f7/mmr-29-06-13213-g02.jpg

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本文引用的文献

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Front Mol Biosci. 2023 Sep 26;10:1258870. doi: 10.3389/fmolb.2023.1258870. eCollection 2023.
2
and Autophagy: Evidence from Studies on Chaperone-Mediated Autophagy in HepG Cancer Cells.自噬:伴侣介导的自噬在 HepG 癌细胞中的研究证据。
Nutr Cancer. 2023;75(10):1822-1847. doi: 10.1080/01635581.2023.2270215. Epub 2023 Nov 30.
3
Integrating Clinical Cancer and PTM Proteomics Data Identifies a Mechanism of ACK1 Kinase Activation.
整合临床癌症和 PTM 蛋白质组学数据鉴定 ACK1 激酶激活的机制。
Mol Cancer Res. 2024 Feb 1;22(2):137-151. doi: 10.1158/1541-7786.MCR-23-0153.
4
Immunoediting of KEAP1-NRF2 mutant tumours is required to circumvent NRF2-mediated immune surveillance.免疫编辑 KEAP1-NRF2 突变肿瘤是规避 NRF2 介导的免疫监视所必需的。
Redox Biol. 2023 Nov;67:102904. doi: 10.1016/j.redox.2023.102904. Epub 2023 Oct 10.
5
HOOKLESS1 acetylates AUTOPHAGY-RELATED PROTEIN18a to promote autophagy during nutrient starvation in Arabidopsis.钩状结构域蛋白 1 乙酰化自噬相关蛋白 18a 以促进拟南芥在营养饥饿时的自噬。
Plant Cell. 2023 Dec 21;36(1):136-157. doi: 10.1093/plcell/koad252.
6
AKIR-1 regulates proteasome subcellular function in .AKIR-1在……中调节蛋白酶体亚细胞功能。 (原句不完整,此译文根据现有内容翻译)
iScience. 2023 Sep 11;26(10):107886. doi: 10.1016/j.isci.2023.107886. eCollection 2023 Oct 20.
7
HBXIP knockdown inhibits FHL2 to promote cycle arrest and suppress cervical cancer cell proliferation, invasion and migration.HBXIP基因敲低抑制FHL2,从而促进细胞周期停滞并抑制宫颈癌细胞的增殖、侵袭和迁移。
Oncol Lett. 2023 Mar 24;25(5):186. doi: 10.3892/ol.2023.13772. eCollection 2023 May.
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HBXIP blocks myosin-IIA assembly by phosphorylating and interacting with NMHC-IIA in breast cancer metastasis.在乳腺癌转移过程中,HBXIP通过磷酸化并与非肌肉肌球蛋白重链-IIA(NMHC-IIA)相互作用来阻断肌球蛋白-IIA的组装。
Acta Pharm Sin B. 2023 Mar;13(3):1053-1070. doi: 10.1016/j.apsb.2022.11.025. Epub 2022 Nov 25.
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