Macrophages and cancer stem cells: a malevolent alliance.
Macrophages and cancer stem cells: a malevolent alliance.
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DOI：
10.1186/s10020-021-00383-3
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发表时间：
2021-09-28
期刊：
影响因子：
--
通讯作者：
Belgiovine C
中科院分区：
文献类型：
--
作者：
Allavena P;Digifico E;Belgiovine C
近年来，由于髓系细胞的促肿瘤和免疫抑制功能与疾病进展和治疗反应密切相关，浸润性肿瘤的髓系细胞日益受到重视。肿瘤相关巨噬细胞(TAMs)的功能不明确是一个具有挑战性的障碍，它主要促进肿瘤的进化。在癌症干细胞(CSCs)的情况下，这一点更加明显；作为癌症干细胞利基的专门环境的积极参与者，TAMS启动了与CSCs的对等对话。TAMs有助于保护CSCs免受恶劣环境(外源性侮辱、有毒化合物、免疫细胞的攻击)的影响，并产生几种生物活性介质，调节维持癌细胞干细胞生长的关键发育途径。在这篇综述中，我们主要关注TAMS和CSCs之间的相互作用；我们描述了TAMS如何影响CSC生物学，进而CSCs如何利用巨噬细胞的组织营养活性来生存和发展。由于CSCs负责治疗抵抗和肿瘤复发，因此它们是重要的治疗靶点。鉴于最近通过刺激免疫系统在肿瘤学方面取得的成功，我们讨论了一些针对巨噬细胞的治疗策略，这些策略也可能影响CSCs并破坏它们的恶意联盟。
Myeloid cells infiltrating tumors are gaining ever growing attention in the last years because their pro-tumor and immunosuppressive functions are relevant for disease progression and therapeutic responses. The functional ambiguity of tumor-associated macrophages (TAMs), mostly promoting tumor evolution, is a challenging hurdle. This is even more evident in the case of cancer stem cells (CSCs); as active participants in the specialized environment of the cancer stem cell niche, TAMs initiate a reciprocal conversation with CSCs. TAMs contribute to protect CSCs from the hostile environment (exogenous insults, toxic compounds, attacks from the immune cells), and produce several biologically active mediators that modulate crucial developmental pathways that sustain cancer cell stemness. In this review, we have focused our attention on the interaction between TAMs and CSCs; we describe how TAMs impact on CSC biology and, in turn, how CSCs exploit the tissue trophic activity of macrophages to survive and progress. Since CSCs are responsible for therapy resistance and tumor recurrence, they are important therapeutic targets. In view of the recent success in oncology obtained by stimulating the immune system, we discuss some macrophage-targeted therapeutic strategies that may also affect the CSCs and interrupt their malevolent alliance.
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源自 M2 肿瘤相关巨噬细胞的 TNF-α 通过 Wnt/β-catenin 通路促进 SMMC-7721 肝癌细胞上皮间质转化和癌症恶化
影响因子：
3.7
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