Effects of blue-light-exposure on growth of extracorporeally circulated leukemic cells in rats with leukemia induced by 1-ethyl-1-nitrosourea

Ohara, Masaru; Kawashima, Yuzo; Watanabe, Haruo; Kitajima, Shunichi

doi:10.3892/ijmm.10.4.407

Cited by 9 publications

(10 citation statements)

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“…Notable among the various species of LED is that blue LED with 430-490 nm wavelengths showed excelent antitumor activity in vitro and in vivo experiments. Blue light could effectively inhibit the tumor progress of skin tumors, melanoma, leukemia, colon cancer mainly depending on the accumulation of intracellular reactive oxygen species (ROS) [8][9][10][11]. Consistent with these reports, our previous study demonstrated that blue LED could enhance the anti-tumor effects of arsenic trioxide on human osteosarcoma and cause cell death in colorectal cancer through increasing ROS accumulation and DNA damaged mediated p53 activation [12,13].…”

Section: Introductionsupporting

confidence: 67%

Blue LED causes cell death in human hepatoma by inducing DNA damage

et al. 2020

Preprint

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Phototherapies, including sunlight, infrared, ultraviolet, visible and laser, parts of which present high curative effect, small invasion, and negligible adverse reactions in cancer treatment. Here we aimed to explore the potential therapeutical effects of blue LED in hepatoma cell and decipher the underlying cellular/molecular mechanisms. We demonstrated that the irradiation of blue LED light in hepatoma cell could lead to cell proliferation reduction along with the cell apoptosis increase. Simultaneously, blue LED irradiation also markedly suppressed the migration and invasion ability of hepatoma cells. Sphere formation analysis further revealed the decreased stemness of hepatoma cell under the treatment of blue LED irradiation. In addition, blue LED irradiation significantly promoted the expression of γ-H2AX, a sensitive molecular marker of DNA damage. Collectively, we demonstrated that blue LED irradiation exhibited anti-tumor effects on liver cancer by inducing DNA damage, representing a potential approach for human hepatoma treatment.

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Section: Introductionsupporting

confidence: 67%

Blue LED causes cell death in human hepatoma by inducing DNA damage

et al. 2020

Preprint

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“…12) Blue light also selectively inhibits the growth of perfused HL60 cells and metastasis of the cells in rats. 13,14) An ideal model for the assessment of the inhibitory effects of blue light on the growth of cancer cells in the clinical setting would be a cancer-bearing animal that has a tumor that is difficult to excise, but is located in a site that is suitable for daily external exposure. Exposure to blue light significantly reduced the incidence rate and number of papillomas induced by TPA application in v-Ha-ras (TG-AC) transgenic mice in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…When the blood of rats with 1-ethyl-1-nitrosourea (ENU)induced leukemia was exposed to blue light for 3 h during extracorporeal circulation, the growth of leukemic cells was suppressed, but the growth of normal lymphocytes did not differ significantly from that of the cells in the control group. 13) Additionally, when B16 melanoma cells that had been exposed to blue light and incubated for 7 days were injected intravenously into mice, it was found that blue light exposure significantly inhibited metastasis of the B16 melanoma cells to the lung. 14) Skin tumors are expected to be one of the targets for treatment by blue light exposure, because the tumors are difficult to excise surgically, but readily accessible to external light exposure.…”

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confidence: 99%

Blue light inhibits the growth of skin tumors in the v‐Ha‐ras transgenic mouse

et al. 2003

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12-O-Tetradecanoylphorbol-13-acetate (TPA) was applied to the back skin of v-Ha-ras (TG-AC) female transgenic mice at a dose of 2.5 µ µ µ µg/200 µ µ µ µl twice a week for 9 weeks. The back skin was then exposed to blue light (wavelength, 470 nm; irradiance, 5.7 mW/ cm 2 ) for 1 h daily for 9 weeks. The mice to which TPA was applied developed skin tumors at 6 weeks after the start of application. The tumor incidence rates at 6, 7, 8 and 9 weeks after the start of application were 70%, 80%, 100% and 100%, respectively, and the numbers of tumors 1 mm or more in diameter were 1, 5, 10 and 19, respectively. In the mice that were exposed to blue light after TPA application, the tumor incidence rates were 10%, 40%, 60% and 80%, respectively, and the numbers of tumors 1 mm or more in diameter were 0, 2, 5 and 9, respectively. Histopathological examination of the skin revealed that TPA application induced diffuse hyperplasia, exaggerated keratinization, and papillomas in all 10 mice. A localized form of epidermal hyperplasia was also observed in 4 mice. The incidence rate of papillomas in the mice that were exposed to blue light after TPA application was lower and the degree of exaggerated keratinization was greater. Exaggerated keratinization was considered to represent a regressive change following exposure.

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“…The effects of blue light appeared to be attributable to the inhibition of DNA synthesis and cell division. When the blood of rats with 1-ethyl-1-nitrosourea (ENU)-induced leukemia was exposed to blue light for 3 h during extracorporeal circulation, the growth of leukemic cells was suppressed, with no significant difference in the growth of normal lymphocytes, compared to the non-exposure control group (13). When B16 melanoma cells exposed to blue light and incubated for 7 days were injected intravenously into mice, the metastasis of B16 melanoma cells to the lung was suppressed (14).…”

Section: Introductionmentioning

confidence: 99%

Augmentation of the inhibitory effect of blue light on the growth of B16 melanoma cells by riboflavin

Ohara

Fujikura²,

Fujiwara³

2003

Int J Oncol

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We have demonstrated that blue light has anticancer effects in cultured cancer cells and tumor-bearing animals. Based on our experimental findings, in addition to cytostatic activity that suppresses the proliferation of B16 melanoma cells, blue light may exert cytocidal activity through interaction with vitamin(s) contained in the culture medium. The present study was undertaken to identify the specific vitamins with which blue light interacts and to investigate the factors responsible for its cytocidal activity. B16 melanoma cells were incubated in media supplemented with various vitamins and exposed to blue light for 10 min. Cell necrosis was observed only in media containing riboflavin (0.4 mg/l). The effects of other components of visible light on riboflavin were also studied. Riboflavin-containing media were exposed to light of each of the three primary colors (red, green and blue) and the effects on the colony-forming capacity of B16 melanoma cells were evaluated. Cell necrosis was induced only in media exposed to blue light. The effects of riboflavin increased in a concentration-dependent manner in the range from 0.3 to 1.0 mg/l in blue-light-exposed media and were antagonized by the presence of catalase (200 U/ml). These findings suggest that cell necrosis is probably induced by active oxygen species such as hydrogen peroxide formed by the reaction of riboflavin with blue light.

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Effects of blue-light-exposure on growth of extracorporeally circulated leukemic cells in rats with leukemia induced by 1-ethyl-1-nitrosourea

Cited by 9 publications

References 0 publications

Blue LED causes cell death in human hepatoma by inducing DNA damage

Blue LED causes cell death in human hepatoma by inducing DNA damage

Blue light inhibits the growth of skin tumors in the v‐Ha‐ras transgenic mouse

Augmentation of the inhibitory effect of blue light on the growth of B16 melanoma cells by riboflavin

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