Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis
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...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-01-01
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| Series: | Life |
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| Online Access: | https://www.mdpi.com/2075-1729/13/2/320 |
| _version_ | 1797619853460242432 |
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| author | Yi-Yuan Lin Shin-Yi Lee Yu-Jung Cheng |
| author_facet | Yi-Yuan Lin Shin-Yi Lee Yu-Jung Cheng |
| author_sort | Yi-Yuan Lin |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-11T08:33:52Z |
| format | Article |
| id | doaj.art-ae3f3acfa465494da5bb61310023b368 |
| institution | Directory Open Access Journal |
| issn | 2075-1729 |
| language | English |
| last_indexed | 2024-03-11T08:33:52Z |
| publishDate | 2023-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Life |
| spelling | doaj.art-ae3f3acfa465494da5bb61310023b3682023-11-16T21:39:38ZengMDPI AGLife2075-17292023-01-0113232010.3390/life13020320Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting AngiogenesisYi-Yuan Lin0Shin-Yi Lee1Yu-Jung Cheng2Department of Exercise and Health Science, National Taipei University of Nursing and Health Sciences, Taipei 112303, TaiwanGeneral Education Center, China Medical University, Taichung 406, TaiwanDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, China Medical University, Taichung 406, TaiwanThe 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.https://www.mdpi.com/2075-1729/13/2/320melanomatumor growthangiogenesislow-level laser therapy |
| spellingShingle | Yi-Yuan Lin Shin-Yi Lee Yu-Jung Cheng Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis Life melanoma tumor growth angiogenesis low-level laser therapy |
| title | Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis |
| title_full | Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis |
| title_fullStr | Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis |
| title_full_unstemmed | Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis |
| title_short | Low-Level Laser Therapy Induces Melanoma Tumor Growth by Promoting Angiogenesis |
| title_sort | low level laser therapy induces melanoma tumor growth by promoting angiogenesis |
| topic | melanoma tumor growth angiogenesis low-level laser therapy |
| url | https://www.mdpi.com/2075-1729/13/2/320 |
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