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低强度激光疗法通过促进血管生成诱导黑色素瘤肿瘤生长。

Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis.

作者信息

Lin Yi-Yuan, Lee Shin-Yi, Cheng Yu-Jung

机构信息

Department of Exercise and Health Science, National Taipei University of Nursing and Health Sciences, Taipei 112303, Taiwan.

General Education Center, China Medical University, Taichung 406, Taiwan.

出版信息

Life (Basel). 2023 Jan 23;13(2):320. doi: 10.3390/life13020320.

DOI:10.3390/life13020320
PMID:36836677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9962383/
Abstract

The effects of low-level laser therapy (LLLT) on tumor growth are inconsistent. In this study, we investigated the effects of LLLT on melanoma tumor growth and angiogenesis. C57/BL6 mice were challenged with B16F10 melanoma cells and treated with LLLT for 5 consecutive days; untreated mice were used as controls. Tumor weight, angiogenesis, immunohistochemistry, and protein levels were compared between the treated and untreated mice. In an in vitro experiment, B16F10 cells were treated with LLLT. Proteins were extracted and subjected to Western blot analysis for analyzing signaling pathways. Compared with the findings in the untreated mice, tumor weight substantially increased in the treated mice. Both immunohistochemical and Western blot analyses revealed markedly increased levels of CD31, a biomarker of vascular differentiation, in the LLLT group. In B16F10 cells, LLLT considerably induced the phosphorylation of extracellular signal-regulated kinase (ERK), which, in turn, phosphorylated p38 mitogen-activated protein kinase (MAPK). Furthermore, LLLT induced the expression of vascular endothelial growth factor, but not hypoxia-inducible factor-1α, through the ERK/p38 MAKP signaling pathways. Our findings indicate that LLLT induces melanoma tumor growth by promoting angiogenesis. Therefore, it should be avoided in patients with melanoma.

摘要

低强度激光疗法(LLLT)对肿瘤生长的影响并不一致。在本研究中,我们调查了LLLT对黑色素瘤肿瘤生长和血管生成的影响。用B16F10黑色素瘤细胞攻击C57/BL6小鼠,并连续5天用LLLT治疗;未治疗的小鼠用作对照。比较治疗组和未治疗组小鼠的肿瘤重量、血管生成、免疫组织化学和蛋白质水平。在体外实验中,用LLLT处理B16F10细胞。提取蛋白质并进行蛋白质印迹分析以分析信号通路。与未治疗小鼠的结果相比,治疗组小鼠的肿瘤重量显著增加。免疫组织化学和蛋白质印迹分析均显示,LLLT组中血管分化生物标志物CD31的水平明显升高。在B16F10细胞中,LLLT显著诱导细胞外信号调节激酶(ERK)的磷酸化,进而使p38丝裂原活化蛋白激酶(MAPK)磷酸化。此外,LLLT通过ERK/p38 MAPK信号通路诱导血管内皮生长因子的表达,但不诱导缺氧诱导因子-1α的表达。我们的研究结果表明,LLLT通过促进血管生成诱导黑色素瘤肿瘤生长。因此,黑色素瘤患者应避免使用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/eb68b252a4f4/life-13-00320-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/2ddd8994987a/life-13-00320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/25b84835332c/life-13-00320-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/1b65f21ffa58/life-13-00320-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/8686dca3218d/life-13-00320-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/33ae78392c46/life-13-00320-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/eb68b252a4f4/life-13-00320-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/2ddd8994987a/life-13-00320-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/25b84835332c/life-13-00320-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/1b65f21ffa58/life-13-00320-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/8686dca3218d/life-13-00320-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/33ae78392c46/life-13-00320-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a610/9962383/eb68b252a4f4/life-13-00320-g006.jpg

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