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海洋天然产物lepadin A作为一种通过CD91依赖性途径诱导免疫原性细胞死亡的新型诱导剂。

Marine natural product lepadin A as a novel inducer of immunogenic cell death via CD91-dependent pathway.

作者信息

Carbone Dalila, Gallo Carmela, Nuzzo Genoveffa, Barra Giusi, Dell'Isola Mario, Affuso Mario, Follero Olimpia, Albiani Federica, Sansone Clementina, Manzo Emiliano, d'Ippolito Giuliana, Fontana Angelo

机构信息

Institute of Biomolecular Chemistry, Consiglio Nazionale Delle Ricerche, Via Campi Flegrei 34, Pozzuoli, 80078, Naples, Italy.

Department of Biology, University of Naples "Federico II", Via Cupa Nuova Cinthia 21, 80126, Naples, Italy.

出版信息

Nat Prod Bioprospect. 2023 Oct 2;13(1):34. doi: 10.1007/s13659-023-00401-3.

Abstract

Immunogenic Cell Death (ICD) represents a mechanism of enhancing T cell-driven response against tumor cells. The process is enabled by release of damage-associated molecular patterns (DAMPs) and cytokines by dying cells. Based on molecular studies and clinical marker assessment, ICD can be a new target for cancer chemotherapy hitherto restricted to a few conventional anticancer drugs. In view of the development of small molecules in targeted cancer therapy, we reported the preliminary evidence on the role of the natural product lepadin A (1) as a novel ICD inducer. Here we describe the ICD mechanism of lepadin A (1) by proving the translocation of the protein calreticulin (CRT) to the plasma membrane of human A2058 melanoma cells. CRT exposure is an ICD marker in clinical studies and was associated with the activation of the intrinsic apoptotic pathway in A2058 cells with lepadin A (1). After the treatment, the tumour cells acquired the ability to activate dendritic cells (DCs) with cytokine release and costimulatory molecule expression that is consistent with a phenotypic profile committed to priming T lymphocytes via a CD91-dependent mechanism. The effect of lepadin A (1) was dose-dependent and comparable to the response of the chemotherapy drug doxorubicin (2), a well-established ICD inducer.

摘要

免疫原性细胞死亡(ICD)是一种增强T细胞驱动的抗肿瘤细胞反应的机制。这一过程是由垂死细胞释放损伤相关分子模式(DAMPs)和细胞因子所促成的。基于分子研究和临床标志物评估,ICD可能成为癌症化疗的一个新靶点,而迄今为止癌症化疗仅限于少数几种传统抗癌药物。鉴于靶向癌症治疗中小分子的发展,我们报道了天然产物海鞘素A(1)作为一种新型ICD诱导剂作用的初步证据。在此,我们通过证实钙网蛋白(CRT)易位至人A2058黑色素瘤细胞的质膜,描述了海鞘素A(1)的ICD机制。在临床研究中,CRT暴露是一种ICD标志物,并且在海鞘素A(1)处理的A2058细胞中,它与内源性凋亡途径的激活相关。处理后,肿瘤细胞获得了通过释放细胞因子和表达共刺激分子来激活树突状细胞(DCs)的能力,这与通过依赖CD91的机制启动T淋巴细胞的表型特征一致。海鞘素A(1)的作用呈剂量依赖性,且与化疗药物阿霉素(2)(一种成熟的ICD诱导剂)的反应相当。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c28/10542626/419aa8e08fc8/13659_2023_401_Fig1_HTML.jpg

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