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P53/NANOG平衡；肝癌细胞中低分化状态与高分化状态之间的主要切换因素。

P53/NANOG balance; the leading switch between poorly to well differentiated status in liver cancer cells.

作者信息

Ranjbar-Niavol Fazeleh, Rezaei Niloufar, Zhao Ying, Mirzaei Hamed, Hassan Moustapha, Vosough Massoud

机构信息

Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, Academic Center for Education, Culture and Research (ACECR), Tehran, Iran.

Experimental Cancer Medicine, Institution for Laboratory Medicine, Karolinska Institute and Karolinska University Hospital-Huddinge, Huddinge, Sweden.

出版信息

Front Oncol. 2024 May 23;14:1377761. doi: 10.3389/fonc.2024.1377761. eCollection 2024.

DOI:10.3389/fonc.2024.1377761
PMID:38846985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11153735/
Abstract

Enforcing a well-differentiated state on cells requires tumor suppressor p53 activation as a key player in apoptosis induction and well differentiation. In addition, recent investigations showed a significant correlation between poorly differentiated status and higher expression of NANOG. Inducing the expression of NANOG and decreasing p53 level switch the status of liver cancer cells from well differentiated to poorly status. In this review, we highlighted p53 and NANOG cross-talk in hepatocellular carcinoma (HCC) which is regulated through mitophagy and makes it a novel molecular target to attenuate cancerous phenotype in the management of this tumor.

摘要

在细胞中强制使其处于高度分化状态需要肿瘤抑制因子p53激活，这是诱导细胞凋亡和实现良好分化的关键因素。此外，最近的研究表明，低分化状态与NANOG的高表达之间存在显著相关性。诱导NANOG的表达并降低p53水平可使肝癌细胞的状态从高分化转变为低分化状态。在本综述中，我们重点介绍了肝细胞癌（HCC）中p53和NANOG的相互作用，这种相互作用通过线粒体自噬进行调节，并使其成为在该肿瘤治疗中减弱癌表型的新型分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/9441b47f84d2/fonc-14-1377761-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/0cebb3274d44/fonc-14-1377761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/2e4a55221b31/fonc-14-1377761-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/9441b47f84d2/fonc-14-1377761-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/0cebb3274d44/fonc-14-1377761-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/2e4a55221b31/fonc-14-1377761-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f24/11153735/9441b47f84d2/fonc-14-1377761-g003.jpg

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本文引用的文献

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Nat Rev Clin Oncol. 2023 Dec;20(12):864-884. doi: 10.1038/s41571-023-00825-3. Epub 2023 Oct 26.
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Autophagy as a Target for Non-Immune Intrinsic Functions of Programmed Cell Death-Ligand 1 in Cancer.自噬作为肿瘤程序性细胞死亡配体 1 非免疫固有功能的靶点。
Int J Mol Sci. 2023 Oct 9;24(19):15016. doi: 10.3390/ijms241915016.
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Therapeutic implications of targeting autophagy and TGF-β crosstalk for the treatment of liver fibrosis.
微小RNA作为肝细胞癌的关键因素：对其在转移中作用的见解
Biochem Genet. 2025 Apr;63(2):1014-1062. doi: 10.1007/s10528-024-10897-0. Epub 2024 Aug 5.
靶向自噬与 TGF-β 相互作用治疗肝纤维化的治疗意义。
Life Sci. 2023 Sep 15;329:121894. doi: 10.1016/j.lfs.2023.121894. Epub 2023 Jun 26.
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Cancer stem cell fate determination: mito-nuclear communication.肿瘤干细胞命运决定：线粒体-核通讯。
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Role of p53 suppression in the pathogenesis of hepatocellular carcinoma.p53抑制在肝细胞癌发病机制中的作用。
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