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肝脏的促转移微环境。

The prometastatic microenvironment of the liver.

作者信息

Vidal-Vanaclocha Fernando

机构信息

Department of Cellular Biology and Histology, School of Medicine and Dentistry, University of the Basque Country, Leioa, Bizkaia, Spain.

出版信息

Cancer Microenviron. 2008 Dec;1(1):113-29. doi: 10.1007/s12307-008-0011-6. Epub 2008 May 17.

Abstract

The liver is a major metastasis-susceptible site and majority of patients with hepatic metastasis die from the disease in the absence of efficient treatments. The intrahepatic circulation and microvascular arrest of cancer cells trigger a local inflammatory reaction leading to cancer cell apoptosis and cytotoxicity via oxidative stress mediators (mainly nitric oxide and hydrogen peroxide) and hepatic natural killer cells. However, certain cancer cells that resist or even deactivate these anti-tumoral defense mechanisms still can adhere to endothelial cells of the hepatic microvasculature through proinflammatory cytokine-mediated mechanisms. During their temporary residence, some of these cancer cells ignore growth-inhibitory factors while respond to proliferation-stimulating factors released from tumor-activated hepatocytes and sinusoidal cells. This leads to avascular micrometastasis generation in periportal areas of hepatic lobules. Hepatocytes and myofibroblasts derived from portal tracts and activated hepatic stellate cells are next recruited into some of these avascular micrometastases. These create a private microenvironment that supports their development through the specific release of both proangiogenic factors and cancer cell invasion- and proliferation-stimulating factors. Moreover, both soluble factors from tumor-activated hepatocytes and myofibroblasts also contribute to the regulation of metastatic cancer cell genes. Therefore, the liver offers a prometastatic microenvironment to circulating cancer cells that supports metastasis development. The ability to resist anti-tumor hepatic defense and to take advantage of hepatic cell-derived factors are key phenotypic properties of liver-metastasizing cancer cells. Knowledge on hepatic metastasis regulation by microenvironment opens multiple opportunities for metastasis inhibition at both subclinical and advanced stages. In addition, together with metastasis-related gene profiles revealing the existence of liver metastasis potential in primary tumors, new biomarkers on the prometastatic microenvironment of the liver may be helpful for the individual assessment of hepatic metastasis risk in cancer patients.

摘要

肝脏是主要的易发生转移的部位,大多数肝转移患者在缺乏有效治疗的情况下会死于该疾病。癌细胞在肝内循环和微血管停滞会引发局部炎症反应,通过氧化应激介质(主要是一氧化氮和过氧化氢)和肝脏自然杀伤细胞导致癌细胞凋亡和细胞毒性。然而,某些抵抗甚至使这些抗肿瘤防御机制失活的癌细胞仍可通过促炎细胞因子介导的机制黏附于肝微血管的内皮细胞。在它们短暂停留期间,其中一些癌细胞无视生长抑制因子,同时对肿瘤激活的肝细胞和窦状细胞释放的增殖刺激因子作出反应。这导致在肝小叶的门周区域产生无血管微转移。接下来,源自门管区的肝细胞和成肌纤维细胞以及活化的肝星状细胞被招募到其中一些无血管微转移灶中。这些细胞创造了一个私密的微环境,通过特异性释放促血管生成因子以及癌细胞侵袭和增殖刺激因子来支持它们的发展。此外,肿瘤激活的肝细胞和成肌纤维细胞释放的可溶性因子也有助于调节转移性癌细胞的基因。因此,肝脏为循环中的癌细胞提供了一个促进转移的微环境,支持转移的发展。抵抗肝脏抗肿瘤防御以及利用肝细胞衍生因子的能力是肝转移癌细胞的关键表型特性。关于微环境对肝转移调节的知识为在亚临床和晚期阶段抑制转移提供了多种机会。此外,连同揭示原发性肿瘤中存在肝转移潜能的转移相关基因谱一起,肝脏促转移微环境的新生物标志物可能有助于对癌症患者肝转移风险进行个体评估。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dba/2654354/077afddd8a89/12307_2008_11_Fig2_HTML.jpg

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