STAT3/BCL-xL轴阻断导致岩藻黄质(一种海洋来源的类胡萝卜素)对人膀胱尿路上皮癌细胞的细胞毒性和顺铂增敏作用。

IF 4.9 2区 医学 Q1 CHEMISTRY, MEDICINAL
Marine Drugs Pub Date : 2025-01-22 DOI:10.3390/md23020054
Wen-Chyi Dai, Tzu-Hsuan Chen, Tzu-Ching Peng, Yung-Ching He, Chao-Yu Hsu, Chia-Che Chang
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引用次数: 0

摘要

膀胱癌是一种全球流行的泌尿系统恶性肿瘤,其中移行性癌(TCC)占大多数病例。顺铂是转移性膀胱癌化疗的主要药物;然而,其应用受到肾毒性和耐药性的限制。信号换能器和转录激活因子3 (STAT3)是一种在各种癌症中经常过度激活的致癌转录因子,使其成为一个有吸引力的药物靶点。岩藻黄素是一种海洋类胡萝卜素,具有显著的抗癌特性。本研究探讨岩藻黄质对人膀胱TCC细胞的细胞毒性作用及其增强顺铂疗效的潜力,以及这些作用的潜在机制。我们通过z- vad - fmark介导的岩藻黄素细胞毒性的消除,证明了岩藻黄素通过诱导细胞凋亡对膀胱TCC细胞具有细胞毒性。此外,岩藻黄素降低了固有的或白素-6诱导的酪氨酸705磷酸化STAT3的水平,同时下调了STAT3的靶点BCL-xL。值得注意的是,STAT3- c(一种显性活性STAT3突变体)或BCL-xL的异位表达阻碍了岩藻黄质的促凋亡和细胞毒性作用。此外,亚毒性剂量的岩藻黄素增强了最初对顺铂耐药的膀胱TCC细胞对顺铂诱导的凋亡的敏感性。值得注意的是,当细胞异位表达STAT3-C或BCL-xL时,岩藻黄素的这种顺铂增敏作用被消除。总的来说,我们首次证明岩藻黄质对人膀胱TCC细胞的促凋亡、细胞毒性和顺铂致敏作用归因于STAT3/BCL-xL轴的阻断。我们的研究结果强调,靶向STAT3/BCL-xL轴是一种消除膀胱TCC细胞和促进顺铂致敏的有希望的策略,并进一步支持将岩藻黄素纳入顺铂基础化疗治疗膀胱癌的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blockade of the STAT3/BCL-xL Axis Leads to the Cytotoxic and Cisplatin-Sensitizing Effects of Fucoxanthin, a Marine-Derived Carotenoid, on Human Bladder Urothelial Carcinoma Cells.

Bladder cancer is a globally prevalent urological malignancy, with transitional carcinoma (TCC) representing the majority of cases. Cisplatin is the primary drug for metastatic bladder cancer chemotherapy; however, its application is limited by nephrotoxicity and resistance. Signal Transducer and Activator of Transcription 3 (STAT3) is an oncogenic transcription factor often overactivated in various cancers, making it an appealing drug target. Fucoxanthin, a marine carotenoid, has significant anticancer properties. This study explored Fucoxanthin's cytotoxic effects and its potential to potentiate the efficacy of Cisplatin, along with the mechanisms underlying these effects, on human bladder TCC cells. We demonstrated that Fucoxanthin is cytotoxic to bladder TCC cells by inducing apoptosis, evidenced by z-VAD-fmk-mediated annulment of Fucoxanthin's cytotoxicity. Furthermore, Fucoxanthin reduced the levels of inherent or interleukin-6-induced tyrosine 705-phosphorylated STAT3 accompanied by downregulating BCL-xL, a well-established STAT3 target. Notably, ectopic expression of STAT3-C, a dominant-active STAT3 mutant, or BCL-xL thwarted Fucoxanthin's proapoptotic and cytotoxic actions. Moreover, Fucoxanthin at subtoxic dosages enhanced the susceptibility to Cisplatin-induced apoptosis of bladder TCC cells initially resistant to Cisplatin. Remarkably, this Cisplatin-sensitizing effect of Fucoxanthin was abrogated when cells ectopically expressed STAT3-C or BCL-xL. Overall, for the first time, we proved that the proapoptotic, cytotoxic, and Cisplatin-sensitizing effects of Fucoxanthin on human bladder TCC cells are attributed to the blockade of the STAT3/BCL-xL axis. Our findings highlight that targeting the STAT3/BCL-xL axis is a promising strategy to eliminate bladder TCC cells and facilitate Cisplatin sensitization, and further support the potential of incorporating Fucoxanthin into Cisplatin-based chemotherapy for treating bladder cancer.

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来源期刊
Marine Drugs
Marine Drugs 医学-医药化学
CiteScore
9.60
自引率
14.80%
发文量
671
审稿时长
1 months
期刊介绍: Marine Drugs (ISSN 1660-3397) publishes reviews, regular research papers and short notes on the research, development and production of drugs from the sea. Our aim is to encourage scientists to publish their experimental and theoretical research in as much detail as possible, particularly synthetic procedures and characterization information for bioactive compounds. There is no restriction on the length of the experimental section.
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