Krzywon Aleksandra, Widel Maria, Fujarewicz Krzysztof, Skonieczna Magdalena, Rzeszowska-Wolny Joanna
Biosystems Group, Institute of Automatic Control, Faculty of Automatics, Electronics and Informatics, Silesian University of Technology, 16 Akademicka Street, 44-100 Gliwice, Poland.
Biosystems Group, Institute of Automatic Control, Faculty of Automatics, Electronics and Informatics, Silesian University of Technology, 16 Akademicka Street, 44-100 Gliwice, Poland.
J Photochem Photobiol B. 2018 Jan;178:505-511. doi: 10.1016/j.jphotobiol.2017.12.012. Epub 2017 Dec 9.
UVA radiation, which accounts for about 95% of the solar spectrum, contributes to and may be the etiological factor of skin cancers of which malignant melanoma is the most aggressive. UVA causes oxidative stress in various types of cells in the skin, keratinocyte, melanocytes, and fibroblasts, which is responsible for its cytotoxic effect. Here we used a transwell system to explore how the responses of melanoma cells to a low dose of UVA (20kJ/m, ~10% of the minimal erythema dose) are influenced by neighboring co-cultured melanoma cells or fibroblasts. This dose had a low toxicity for melanoma cells, but after irradiation, co-culture with non-irradiated melanoma cells caused a strong decline in their viability and an increased frequency of apoptosis, whereas co-culture with fibroblast exerted a protective effect on irradiated melanoma cells. At the same time, the presence of non-irradiated cells, especially fibroblasts, decreased the level of UVA-induced reactive oxygen and nitrogen species. Interleukins efficiently produced by fibroblasts seem to be main players in these effects. Our studies reveal that coexistence of fibroblasts with melanoma cells may strongly modulate the direct action and may change bystander effects exerted by UVA light. Similar modulation of the effect of UVA on melanoma cells in vivo by bystander-like signaling from neighboring cells would have consequences for the development of malignant melanoma.
紫外线A辐射约占太阳光谱的95%，它与皮肤癌的发生有关，可能是其病因，其中恶性黑色素瘤最为侵袭性。紫外线A会在皮肤的各种细胞（角质形成细胞、黑素细胞和成纤维细胞）中引起氧化应激，这是其细胞毒性作用的原因。在这里，我们使用Transwell系统来探究低剂量紫外线A（20kJ/m，约为最小红斑剂量的10%）对黑色素瘤细胞的影响是如何受到相邻共培养的黑色素瘤细胞或成纤维细胞影响的。这个剂量对黑色素瘤细胞毒性较低，但照射后，与未照射的黑色素瘤细胞共培养会导致其活力大幅下降，凋亡频率增加，而与成纤维细胞共培养则对照射后的黑色素瘤细胞起到保护作用。同时，未照射细胞，尤其是成纤维细胞的存在，会降低紫外线A诱导的活性氧和氮物种水平。成纤维细胞高效产生的白细胞介素似乎是这些效应的主要参与者。我们的研究表明，成纤维细胞与黑色素瘤细胞共存可能会强烈调节直接作用，并可能改变紫外线A光产生的旁观者效应。邻近细胞类似旁观者的信号对体内紫外线A对黑色素瘤细胞作用的类似调节将对恶性黑色素瘤的发展产生影响。
