"Stromal cells in prostate cancer pathobiology: friends or foes?".
"Stromal cells in prostate cancer pathobiology: friends or foes?".
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DOI：
10.1038/s41416-022-02085-x
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发表时间：
2023-04
影响因子：
8.8
通讯作者：
Loda M
中科院分区：
文献类型：
--
作者：
Pederzoli F;Raffo M;Pakula H;Ravera F;Nuzzo PV;Loda M
前列腺癌病理学的基因组、表观遗传和代谢决定因素已在上皮癌细胞中得到广泛研究。然而，恶性细胞不断与周围环境（即所谓的肿瘤微环境（TME））相互作用，这可能会影响肿瘤细胞增殖和侵袭或饥饿和死亡。在这方面，基质细胞（包括成纤维细胞、平滑肌细胞和脉管系统相关细胞）构成了前列腺癌 TME 的重要组成部分。然而，与其他细胞类型（即免疫细胞）相比，它们在很大程度上被忽视了。事实上，它们在前列腺生理学中的重要性始于器官发生，因为即将形成的前列腺基质决定胚胎上皮细胞致力于前列腺分化。在生命的后期，反应性基质的出现与上皮细胞的恶性转化和癌症进展有关。在这篇综述中，我们讨论了前列腺基质的主要间充质细胞群，强调了它们在健康前列腺上皮向癌症转变中的动态作用。彻底了解这些人群、他们的表型和转录程序可能会提高我们对前列腺癌病理学的理解，并可能有助于利用前列腺基质作为患者分层的生物标志物和治疗靶点。
The genomic, epigenetic and metabolic determinants of prostate cancer pathobiology have been extensively studied in epithelial cancer cells. However, malignant cells constantly interact with the surrounding environment—the so-called tumour microenvironment (TME)—which may influence tumour cells to proliferate and invade or to starve and die. In that regard, stromal cells—including fibroblasts, smooth muscle cells and vasculature-associated cells—constitute an essential fraction of the prostate cancer TME. However, they have been largely overlooked compared to other cell types (i.e. immune cells). Indeed, their importance in prostate physiology starts at organogenesis, as the soon-to-be prostate stroma determines embryonal epithelial cells to commit toward prostatic differentiation. Later in life, the appearance of a reactive stroma is linked to the malignant transformation of epithelial cells and cancer progression. In this Review, we discuss the main mesenchymal cell populations of the prostate stroma, highlighting their dynamic role in the transition of the healthy prostate epithelium to cancer. A thorough understanding of those populations, their phenotypes and their transcriptional programs may improve our understanding of prostate cancer pathobiology and may help to exploit prostate stroma as a biomarker of patient stratification and as a therapeutic target.
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