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同时抑制热休克蛋白和自噬可增强肝癌的射频消融效果。

Simultaneous inhibition of heat shock proteins and autophagy enhances radiofrequency ablation of hepatocellular carcinoma.

机构信息

Department of General Surgery, The Fourth Affiliated Hospital, International Institutes of Medicine, Zhejiang University School of Medicine, Yiwu, 322000, China.

MOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, 310058, China.

出版信息

Biomater Sci. 2024 Nov 19;12(23):6082-6098. doi: 10.1039/d4bm01190b.

Abstract

Radiofrequency ablation (RFA) is a commonly used minimally invasive treatment for hepatocellular carcinoma (HCC). However, incomplete radiofrequency ablation (iRFA) promotes tumor progression and metastasis. There is an urgent need to develop innovative strategies to enhance the efficacy of iRFA. The upregulation of heat shock proteins (HSPs) and activation of protective autophagy in tumor cells upon exposure to sublethal heat enhance the thermotolerance, thereby promoting tumor cell survival. Here, 3-methyladenine (3-MA) and lonidamine (LND) co-encapsulated liposomes (Lip@LND/3-MA) are designed to enhance the efficacy of iRFA by simultaneous inhibition of glycolysis and autophagy. On one hand, LND inhibits hexokinase, a key enzyme in glycolysis, and thus reduces ATP production and consequently suppresses the expression of HSPs. On the other hand, 3-MA, as an autophagy inhibitor, can inhibit protective autophagy after iRFA. Lip@LND/3-MA is confirmed to suppress the expression of HSPs and reduce the autophagy level during RFA. Therefore, the thermotolerance of tumor cells is significantly weakened, leading to remarkably enhanced therapeutic efficacy of iRFA. It is believed that simultaneous inhibition of HSPs and autophagy is a promising therapeutic strategy in clinical practice of RFA.

摘要

射频消融(RFA)是一种常用于治疗肝细胞癌(HCC)的微创治疗方法。然而,不完全射频消融(iRFA)会促进肿瘤的进展和转移。因此,迫切需要开发创新策略来提高 iRFA 的疗效。肿瘤细胞在亚致死热暴露下上调热休克蛋白(HSPs)并激活保护性自噬,从而增强热耐受性,促进肿瘤细胞存活。在这里,设计了 3-甲基腺嘌呤(3-MA)和 Lonidamine(LND)共包封脂质体(Lip@LND/3-MA),通过同时抑制糖酵解和自噬来提高 iRFA 的疗效。一方面,LND 抑制糖酵解的关键酶己糖激酶,从而减少 ATP 的产生,进而抑制 HSPs 的表达。另一方面,3-MA 作为自噬抑制剂,可在 iRFA 后抑制保护性自噬。Lip@LND/3-MA 被证实可在 RFA 期间抑制 HSPs 的表达并降低自噬水平。因此,肿瘤细胞的耐热性显著减弱,导致 iRFA 的治疗效果显著增强。人们相信,同时抑制 HSPs 和自噬是 RFA 临床实践中一种有前途的治疗策略。

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