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Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells

机译:维生素K3与UVB相结合对皮肤鳞状细胞癌的增殖和凋亡的影响A431细胞

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Purpose: Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer and its incidence continues to rise yearly. Photodynamic therapy (PDT) is a non-invasive form of cancer therapy, which utilizes the combined action of a photosensitizer, light, and oxygen molecules to selectively cause cellular damage to tumor cells. Vitamin K3 (VitK3) has been shown to induce apoptosis and inhibit the growth of tumor cells in humans. The purpose of this study was to determine the effect of VitK3 and ultraviolet radiation B (UVB) on oxidative damage, proliferation and apoptosis of A431 cells. Methods: CCK-8 assay was used to detect cell proliferation; Hoechst staining, TUNEL assay and flow cytometry analysis were used to detect apoptosis. Western Blot was perfomed to measure the expression of apoptosis-related proteins. Flow cytometry analysis was employed to detect the reactive oxygen species (ROS) levels and mitochondrial membrane potential. Finally, the role of VitK3 in combination with UVB on the proliferation and apoptosis of A431 cells was investigated using mice xenograft models. Results: We found that the co-treatment of VitK3 combined with UVB more significantly inhibited the growth and proliferation of A431 cells than either VitK3 or UVB alone. Hoechst 33258 staining and flow cytometry analysis revealed that apoptosis was more pronounced in the VitK3-UVB group compared to the VitK3 and UVB groups. Moreover, flow cytometry analysis showed that ROS and the depolarization of the mitochondrial membrane potential were higher in all the co-treatment groups compared to the control, VitK3, and UVB groups. The VitK3-UVB group exhibited a significantly lower tumor growth rate in mouse xenograft models. Conclusion: This study reveals that VitK3 combined with UVB inhibits the growth and induces apoptosis of A431 cells in vitro and suppresses tumor growth and promotes apoptosis of cSCC in vivo.
机译:目的:皮肤鳞状细胞癌(CSCC)是第二种最常见的皮肤癌形式,其发病率继续上升。光动力疗法(PDT)是一种非侵入性癌症治疗形式,其利用光敏剂,光和氧分子的组合作用来选择性地导致肿瘤细胞的细胞损伤。已经显示维生素K3(VIVK3)诱导细胞凋亡并抑制人类肿瘤细胞的生长。本研究的目的是确定Vitk3和紫外线辐射B(UVB)对A431细胞氧化损伤,增殖和凋亡的影响。方法:CCK-8测定用于检测细胞增殖; Hoechst染色,Tunel测定和流式细胞术分析用于检测细胞凋亡。 Western印迹是为了测量凋亡相关蛋白的表达。使用流式细胞术分析来检测反应性氧物质(ROS)水平和线粒体膜电位。最后,使用小鼠异种移植模型研究了VITK3与UVB对UVB的增殖和凋亡的作用。结果:我们发现VITK3与UVB联合的同步抑制了S431细胞的生长和增殖,而不是单独的VITK3或UVB。 Hoechst 33258染色和流式细胞术分析显示,与Vitk3和UVB组相比,Vitk3-UVB组中的细胞凋亡更加明显。此外,流式细胞术分析表明,与对照,VITK3和UVB组相比,所有共处理组的ROS和线粒体膜电位的去极化均较高。 Vitk3-UVB组在小鼠异种移植模型中表现出显着降低的肿瘤生长速率。结论:本研究表明,VITK3与UVB结合抑制了体外肿瘤生长的生长并诱导肿瘤生长,促进体内CSCC的凋亡。

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