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首页> 外文期刊>Otolaryngology--head and neck surgery: official journal of American Academy of Otolaryngology-Head and Neck Surgery >Fenretinide-induced apoptosis of human head and neck squamous carcinoma cell lines.
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Fenretinide-induced apoptosis of human head and neck squamous carcinoma cell lines.

机译：芬维A胺诱导的人头颈部鳞状细胞癌细胞凋亡。

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BACKGROUND: Squamous cell carcinoma of the head and neck (HNSCC) has a high incidence of recurrence and associated second primary malignancy. The retinoid 13-cis-retinoic acid has been shown to be effective as both a chemopreventive and chemotherapeutic agent for HNSCC, but often with treatment-limiting toxicity. The synthetic retinoid fenretinide (N-(4-hydroxyphenyl)retinamide) (HPR) has significant antiproliferative activity against a number of animal and human malignancies and has been used in clinical trials as a chemopreventive agent in patients with breast and prostate cancer and oral leukoplakia. HPR has been shown to have a toxicity profile lower than that for other retinoids used in clinical trials. PURPOSE: The aim of this study was to investigate the effect of HPR on the growth of HNSCC cell lines in vitro. METHODS: Four HNSCC cell lines (JHU-011-SCC, JHU-020-SCC, JHU-022-SCC, and FaDu) were treated with a range of concentrations of HPR for various times. After HPR exposure, cell viability was determined by tetrazolium dye (MTT) colorimetric assay, comparing cell survival with that of untreated control cells. HPR-induced apoptosis was determined by flow-cytometric deoxyribonucleic acid cell-cycle analysis, ultrastructural analysis with electron microscopy, and deoxyribonucleic acid fragmentation detected by gel electrophoresis. RESULTS: HPR caused significant growth inhibition in three of the four HNSCC cell lines in a dose- and time-dependent fashion. In two cell lines (JHU-011-SCC, JHU-020-SCC) a significant antiproliferative effect was achieved between 1 and 2.5 micromol/L HPR after 72 hours of treatment. By deoxyribonucleic acid cell-cycle analysis, electron microscopy, and gel electrophoresis, HPR was shown to induce apoptosis in the JHU-011-SCC and JHU-020-SCC cell lines, but not in the FaDu cell line, which was insensitive to the growth inhibitory effect of HPR. CONCLUSIONS: This study has demonstrated that HPR reduces cell viability in HNSCC cells in vitro at clinically relevant doses, with the growth inhibition occurring through the induction of apoptosis.
机译：背景：头颈部鳞状细胞癌（HNSCC）复发率高，并伴有第二原发恶性肿瘤。类视黄醇13-顺-视黄酸已被证明既可作为HNSCC的化学预防剂也可作为化学治疗剂，但通常具有限制治疗的毒性。合成类维生素A芬维A（N-（4-羟苯基）维酰胺）（HPR）对多种动物和人类恶性肿瘤具有显着的抗增殖活性，并已在临床试验中用作乳腺癌，前列腺癌和口腔白斑患者的化学预防剂。 HPR已显示出比临床试验中使用的其他类维生素A更低的毒性。目的：本研究的目的是研究HPR对体外HNSCC细胞系生长的影响。方法：将四种HNSCC细胞系（JHU-011-SCC，JHU-020-SCC，JHU-022-SCC和FaDu）用一定浓度的HPR进行不同时间的处理。暴露于HPR后，通过四唑鎓染料（MTT）比色测定法确定细胞生存力，将细胞存活率与未处理的对照细胞进行比较。 HPR诱导的凋亡通过流式细胞术脱氧核糖核酸细胞周期分析，电子显微镜超微结构分析以及凝胶电泳检测到的脱氧核糖核酸片段来确定。结果：HPR在四个HNSCC细胞系中的三个中以剂量和时间依赖性方式引起显着的生长抑制。处理72小时后，在两个细胞系（JHU-011-SCC，JHU-020-SCC）中，在1至2.5 micromol / L HPR之间实现了显着的抗增殖作用。通过脱氧核糖核酸细胞周期分析，电子显微镜和凝胶电泳显示，HPR可以诱导JHU-011-SCC和JHU-020-SCC细胞系凋亡，但不会诱导FaDu细胞系凋亡，因为FaDu细胞系对HPD不敏感。 HPR的生长抑制作用。结论：这项研究表明，在临床相关剂量下，HPR降低了HNSCC细胞的细胞活力，并且通过诱导细胞凋亡来抑制生长。

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