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旁观者 Me45 黑素瘤细胞增加 UVC 照射细胞的损伤效应。

Bystander Me45 Melanoma Cells Increase Damaging Effect in UVC-irradiated Cells.

机构信息

Biosystems Group, Faculty of Automatics, Electronics and Informatics, Institute of Automatic Control, Silesian University of Technology, Gliwice, Poland.

出版信息

Photochem Photobiol. 2019 Jul;95(4):1019-1028. doi: 10.1111/php.13080. Epub 2019 Feb 20.

Abstract

The aim of our study was to investigate the possible mechanism(s) of the bystander effect induced by UVC light in malignant melanoma Me45 cells that were co-incubated with irradiated cells of the same line. We have found that the UVC band effectively generated apoptosis, premature senescence, single and double DNA strand breaks and reduced clonogenic survival of bystander cells. However, in the feedback response, the bystander cells intensified damage in directly irradiated cells, especially seen at the level of apoptosis and survival of clonogenic cells. Pretreatment of bystander cells with inhibitor of inducible nitric oxide synthase blocks this signaling. It seems that the mediators of this phenomenon produced and secreted by neighboring cells are superoxide, nitric oxide and TGF-β. The reverse deleterious effect caused by cells not exposed to UVC in directly exposed cells is opposed to the protective/rescue effect exerted by the bystander cells in the case of ionizing radiation known in the literature. Whether this opposite adverse effect is a feature of only Me45 melanoma cells or whether it is a general phenomenon occurring between cells of other types exposed to ultraviolet radiation requires further research.

摘要

我们的研究目的是探讨共培养条件下 UVC 光诱导恶性黑色素瘤 Me45 细胞旁观者效应的可能机制。我们发现 UVC 带有效地诱导旁观者细胞发生凋亡、过早衰老、单链和双链 DNA 断裂,并降低克隆细胞的存活能力。然而,在反馈反应中,旁观者细胞加剧了直接照射细胞的损伤,尤其是在凋亡和克隆细胞存活水平上。用诱导型一氧化氮合酶抑制剂预处理旁观者细胞可以阻断这种信号转导。这种现象的介质可能是由邻近细胞产生和分泌的超氧阴离子、一氧化氮和 TGF-β。与文献中已知的电离辐射情况下旁观者细胞发挥的保护/挽救效应相反,未直接暴露于 UVC 的细胞对直接暴露于 UVC 的细胞造成的这种反向有害效应。这种相反的不利效应是否只是 Me45 黑色素瘤细胞的特征,还是其他类型的细胞在暴露于紫外线辐射时发生的普遍现象,需要进一步研究。

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