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甲状腺癌干细胞:从微环境龛位到治疗策略

Thyroid Cancer Stem-Like Cells: From Microenvironmental Niches to Therapeutic Strategies.

作者信息

Grassi Elisa Stellaria, Ghiandai Viola, Persani Luca

机构信息

Department of Medical Biotechnology and Translational Medicine, University of Milan, 20129 Milan, Italy.

Laboratory of Endocrine and Metabolic Research, Istituto Auxologico Italiano IRCCS, 20149 Milan, Italy.

出版信息

J Clin Med. 2021 Apr 1;10(7):1455. doi: 10.3390/jcm10071455.

DOI:10.3390/jcm10071455
PMID:33916320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8037626/
Abstract

Thyroid cancer (TC) is the most common endocrine malignancy. Recent progress in thyroid cancer biology revealed a certain degree of intratumoral heterogeneity, highlighting the coexistence of cellular subpopulations with distinct proliferative capacities and differentiation abilities. Among those subpopulations, cancer stem-like cells (CSCs) are hypothesized to drive TC heterogeneity, contributing to its metastatic potential and therapy resistance. CSCs principally exist in tumor areas with specific microenvironmental conditions, the so-called stem cell niches. In particular, in thyroid cancer, CSCs' survival is enhanced in the hypoxic niche, the immune niche, and some areas with specific extracellular matrix composition. In this review, we summarize the current knowledge about thyroid CSCs, the tumoral niches that allow their survival, and the implications for TC therapy.

摘要

甲状腺癌(TC)是最常见的内分泌恶性肿瘤。甲状腺癌生物学的最新进展揭示了一定程度的肿瘤内异质性,突出了具有不同增殖能力和分化能力的细胞亚群的共存。在这些亚群中,癌症干细胞样细胞(CSCs)被认为是导致TC异质性的原因,促成了其转移潜能和治疗抗性。CSCs主要存在于具有特定微环境条件的肿瘤区域,即所谓的干细胞龛。特别是在甲状腺癌中,CSCs在缺氧龛、免疫龛以及一些具有特定细胞外基质组成的区域中存活率会提高。在本综述中,我们总结了关于甲状腺CSCs、使其得以存活的肿瘤龛以及对TC治疗的影响的当前知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/ec15342c4f64/jcm-10-01455-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/3ed09ed32d05/jcm-10-01455-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/638c39cbc537/jcm-10-01455-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/ec15342c4f64/jcm-10-01455-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/3ed09ed32d05/jcm-10-01455-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/638c39cbc537/jcm-10-01455-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d23/8037626/ec15342c4f64/jcm-10-01455-g003.jpg

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本文引用的文献

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The p53-induced RNA-binding protein ZMAT3 is a splicing regulator that inhibits the splicing of oncogenic CD44 variants in colorectal carcinoma.p53 诱导的 RNA 结合蛋白 ZMAT3 是一种剪接调节剂,可抑制结直肠癌细胞中致癌性 CD44 变体的剪接。
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