The interplay between cancer associated fibroblasts and immune cells in the context of radiation therapy.
The interplay between cancer associated fibroblasts and immune cells in the context of radiation therapy.
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DOI：
10.1002/mc.23205
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发表时间：
2020-07
影响因子：
4.6
通讯作者：
Karam SD
中科院分区：
文献类型：
--
作者：
Piper M;Mueller AC;Karam SD
成纤维细胞是肿瘤微环境（TME）的关键组成部分，可以作为肿瘤细胞迁移的支架，增强肿瘤承受恶劣条件的能力。当被外部或内源性刺激激活时，正常的成纤维细胞变成癌症相关的成纤维细胞（CAFs），这是肿瘤中异质的一组基质细胞，在表型和表观遗传上与正常的成纤维细胞不同。癌细胞、免疫细胞和CAFs之间通过趋化因子和表面信号的动态串扰使得TME有利于肿瘤生长。当被激活时，CAFs通过调节肿瘤免疫、TME代谢重编程、细胞外基质重塑和收缩以及诱导治疗抵抗等多种现象促进肿瘤发生和转移。电离辐射（放疗[RT]）是一种有效的免疫兴奋剂，已被证明可以增加细胞毒性Teff浸润和IFN-I刺激基因。然而，RT无法克服免疫抑制细胞的浸润和激活，从而促进肿瘤的进展。RT的另一个矛盾之处在于，虽然它在杀死癌细胞方面非常有效，但它可以促进caf的形成。本文综述了在RT过程中CAFs和免疫细胞之间的相互作用如何促进器官纤维化、免疫抑制和肿瘤生长。我们专注于靶向CAF形成的机制途径，作为一种潜在的有效策略，不仅可以预防器官纤维化，还可以在对RT的反应中阻碍肿瘤进展。
Fibroblasts are a key component of the tumor microenvironment (TME) that can serve as a scaffold for tumor cell migration and augment the tumor’s ability to withstand harsh conditions. When activated by external or endogenous stimuli, normal fibroblasts become cancer associated fibroblasts (CAFs), a heterogeneous group of stromal cells in the tumor that are phenotypically and epigenetically different from normal fibroblasts. Dynamic crosstalk between cancer cells, immune cells, and CAFs through chemokines and surface signaling makes the TME conducive to tumor growth. When activated, CAFs promote tumorigenesis and metastasis through several phenomena including regulation of tumor immunity, metabolic reprogramming of the TME, extracellular matrix remodeling and contraction, and induction of therapeutic resistance. Ionizing radiation (radiation theraphy [RT]) is a potent immunological stimulant that has been shown to increase cytotoxic Teff infiltration and IFN-I stimulated genes. RT, however, is unable to overcome the infiltration and activation of immunosuppressive cells which can contribute to tumor progression. Another paradox of RT is that, while very effective at killing cancer cells, it can contribute to the formation of CAFs. This review examines how the interplay between CAFs and immune cells during RT contributes to organ fibrosis, immunosuppression, and tumor growth. We focus on targeting mechanistic pathways of CAF formation as a potentially effective strategy not only for preventing organ fibrosis, but also in hampering tumor progression in response to RT.
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低剂量辐射诱导人间充质基质细胞的衰老并损害自噬过程。
影响因子：
--
作者：
Alessio N;Del Gaudio S;Capasso S;Di Bernardo G;Cappabianca S;Cipollaro M;Peluso G;Galderisi U
通讯作者：
Galderisi U
DOI：
10.3109/08977194.2011.595714
发表时间：
2011-10
期刊：
Growth factors (Chur, Switzerland)
影响因子：
--
作者：
Biernacka A;Dobaczewski M;Frangogiannis NG
通讯作者：
Frangogiannis NG
DOI：
10.1016/j.ijrobp.2013.10.019
发表时间：
2014-01-01
影响因子：
7
作者：
Christensen, Michael;Najy, Abdo J.;Kim, Hyeong-Reh Choi
通讯作者：
Kim, Hyeong-Reh Choi
影响因子：
6.7
作者：
Balogh, Andrea;Persa, Eszter;Lumniczky, Katalin
通讯作者：
Lumniczky, Katalin
影响因子：
3.6
作者：
Chen, He;Yang, Wei-Wei;Chen, Ming
通讯作者：
Chen, Ming