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猕猴桃提取物在治疗黑色素瘤中的潜在用途。

Potential use of kiwifruit extract for treatment of melanoma.

机构信息

Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, 50312, USA.

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA.

出版信息

Med Oncol. 2021 Feb 14;38(3):25. doi: 10.1007/s12032-021-01465-2.

DOI:10.1007/s12032-021-01465-2
PMID:33586074
Abstract

Skin cancers are the most common cancers in the world and among the different types of skin cancers, melanoma is the deadliest and incidence is rising. Previous studies have shown promising in vitro and human evidence of kiwifruit exhibiting anti-cancer effects. This study was designed to investigate if kiwifruit extract (KE) has any effect on CRL-11147 melanoma cancer cells and to investigate the possible mechanisms behind the results. The effects of KE on CRL-11147 melanoma cell survival, proliferation, and apoptosis was investigated using clonogenic survival assay, cell proliferation, and caspase-3 activity kits. Potential anti-tumor molecular mechanisms were elucidated using RT-PCR and IHC. Addition of KE decreased CRL-11147 cell colonies percentages indicated by a decreased optical density value of cancer cells when compared to control. Furthermore, treatment with KE increased relative caspase-3 activity in cancer cells, which indicated increased apoptosis of cancer cells. The anti-proliferative effect of KE on cancer cells corresponded with decreased expression of the pro-proliferative molecule Cyclin E and CDK4, while increased expression of the pro-apoptotic molecule TRAILR1 corresponded with the pro-apoptotic effect. KE decreases CRL-11147 melanoma cell growth via downregulation of Cyclin E and CDK4 and upregulation in TRAILR1. Our study suggests a potential use for KE in treatment of melanoma.

摘要

皮肤癌是世界上最常见的癌症,在不同类型的皮肤癌中,黑色素瘤的死亡率最高,发病率也在上升。先前的研究已经表明,猕猴桃在体外和人体中都具有有希望的抗癌效果。本研究旨在探讨猕猴桃提取物(KE)是否对 CRL-11147 黑色素瘤癌细胞有任何影响,并探讨结果背后的可能机制。使用集落形成生存试验、细胞增殖和 caspase-3 活性试剂盒研究 KE 对 CRL-11147 黑色素瘤细胞存活、增殖和细胞凋亡的影响。使用 RT-PCR 和 IHC 阐明了潜在的抗肿瘤分子机制。与对照组相比,KE 的添加降低了 CRL-11147 细胞集落的百分比,这表明癌细胞的光密度值降低。此外,用 KE 处理增加了癌细胞中相对 caspase-3 的活性,这表明癌细胞的凋亡增加。KE 对癌细胞的抗增殖作用与促增殖分子细胞周期蛋白 E 和 CDK4 的表达降低相对应,而促凋亡分子 TRAILR1 的表达增加与促凋亡作用相对应。KE 通过下调细胞周期蛋白 E 和 CDK4 以及上调 TRAILR1 来减少 CRL-11147 黑色素瘤细胞的生长。我们的研究表明,KE 在治疗黑色素瘤方面具有潜在的用途。

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