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首页> 外文期刊>Journal of Translational Medicine >Periostin involved in the activated hepatic stellate cells-induced progression of residual hepatocellular carcinoma after sublethal heat treatment: its role and potential for therapeutic inhibition
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Periostin involved in the activated hepatic stellate cells-induced progression of residual hepatocellular carcinoma after sublethal heat treatment: its role and potential for therapeutic inhibition

机译：亚致死性热处理后骨膜素参与活化的肝星状细胞诱导的残余肝细胞癌进展：其作用和潜在的治疗抑制作用

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摘要

Incomplete thermal ablation may induce invasiveness of hepatocellular carcinoma (HCC). Here, we investigated whether activated hepatic stellate cells (HSCs) would accelerate the progression of residual HCC after sublethal heat treatment, and thus sought?to identify the?potential?targets. Hepatocellular carcinoma cells were exposed to sublethal heat treatment and then cultured with the conditioned medium from activated HSCs (HSC-CM). The cell proliferation, migration, invasion and parameters of epithelial–mesenchymal transition (EMT) were analyzed. In vivo tumor progression of heat-treated residual HCC cells inoculated with activated HSCs was studied in nude mice. HSC-CM significantly enhanced the proliferation, motility, invasion, prominent EMT activation and decreased apoptosis of heat-exposed residual HCC cells. These increased malignant phenotypes were markedly attenuated by neutralizing periostin (POSTN) in HSC-CM. Furthermore, exogenous POSTN administration exerted the similar effects of HSC-CM on heat-treated residual HCC cells. POSTN induced the prominent activation of p52Shc and ERK1/2 via integrin β1 in heat-exposed residual HCC cells. Vitamin D analog calcipotriol blocked POSTN secretion from activated HSCs. Calcipotriol plus cisplatin significantly suppressed the activated HSCs-enhanced tumor progression of heat-treated residual HCC cells via the inhibited POSTN expression and the increased apoptosis. Activated HSCs promote the tumor progression of heat-treated residual HCC through the release of POSTN, which could be inhibited by calcipotriol. Calcipotriol plus cisplatin could be used to thwart the accelerated progression of residual HCC after suboptimal heat treatment.
机译：不完全的热消融可能会诱发肝细胞癌（HCC）的浸润性。在这里，我们研究了活化的肝星状细胞（HSC）是否会加速亚致死性热处理后残余HCC的进程，从而寻求确定“潜在”靶标。肝癌细胞接受亚致死性热处理，然后与来自活化HSC（HSC-CM）的条件培养基一起培养。分析了上皮-间质转化（EMT）的细胞增殖，迁移，侵袭和参数。在裸鼠中研究了用活化的HSC接种的热处理过的残留HCC细胞的体内肿瘤进展。 HSC-CM显着增强了受热暴露的残留HCC细胞的增殖，运动，侵袭，显着的EMT活化和减少的细胞凋亡。这些增加的恶性表型通过中和HSC-CM中的骨膜素（POSTN）而明显减弱。此外，外源性POSTN给药对热处理后的残留HCC细胞具有类似的HSC-CM作用。 POSTN在暴露于热的残留HCC细胞中通过整联蛋白β1诱导p52Shc和ERK1 / 2的显着激活。维生素D类似物卡泊三醇阻断了活化HSC的POSTN分泌。钙泊三醇加顺铂通过抑制POSTN表达和增加细胞凋亡来显着抑制热处理的残留HCC细胞的活化HSCs增强的肿瘤进程。活化的HSC通过POSTN的释放来促进热处理后残留HCC的肿瘤进展，而后者可能被卡泊三醇抑制。卡泊三醇加顺铂可用于抑制次最佳热处理后残余肝癌的加速进展。

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