Low-power 808-nm laser irradiation inhibits cell proliferation of a human-derived glioblastoma cell line in vitro

Murayama, Hirokazu; Sadakane, Kei; Yamanoha, Banri; Kogure, Shinichi

doi:10.1007/s10103-011-0924-z

Cited by 43 publications

(36 citation statements)

References 31 publications

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“…PBM (808 nm; 5.85 and 7.8 J/cm 2 ) had an inhibitory effect on the proliferation of a human hepatoma cell line [86], and Sroka et al [87] reported that glioblastoma/astrocytoma cells exhibited a slightly decreased mitotic rate after PBM at 805 nm and 5–20 J/cm 2 . Similarly, 808-nm laser irradiation with an energy density of more than 5 J/cm 2 inhibited cell proliferation of glioblastoma cells in vitro [88]. Moreover, Al Watban et al [89] observed growth inhibition of cancer cell lines at relatively high cumulative PBM doses.…”

Section: Pbm Effects On Tumor Cell Linesmentioning

confidence: 99%

Low level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 1: mechanisms of action, dosimetric, and safety considerations

Zecha

Raber-Durlacher

Nair

et al. 2016

Support Care Cancer

208

140

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Purpose There is a large body of evidence supporting the efficacy of low level laser therapy (LLLT), more recently termed photobiomodulation (PBM), for the management of oral mucositis (OM) in patients undergoing radiotherapy for head and neck cancer (HNC). Recent advances in PBM technology, together with a better understanding of mechanisms involved, may expand the applications for PBM in the management of other complications associated with HNC treatment. This article (part 1) describes PBM mechanisms of action, dosimetry, and safety aspects and, in doing so, provides a basis for a companion paper (part 2) which describes the potential breadth of potential applications of PBM in the management of side-effects of (chemo)radiation therapy in patients being treated for HNC and proposes PBM parameters. Methods This study is a narrative non-systematic review. Results We review PBM mechanisms of action and dosimetric considerations. Virtually, all conditions modulated by PBM (e.g., ulceration, inflammation, lymphedema, pain, fibrosis, neurological and muscular injury) are thought to be involved in the pathogenesis of (chemo)radiation therapy-induced complications in patients treated for HNC. The impact of PBM on tumor behavior and tumor response to treatment has been insufficiently studied. In vitro studies assessing the effect of PBM on tumor cells report conflicting results, perhaps attributable to inconsistencies of PBM power and dose. Nonetheless, the biological bases for the broad clinical activities ascribed to PBM have also been noted to be similar to those activities and pathways associated with negative tumor behaviors and impeded response to treatment. While there are no anecdotal descriptions of poor tumor outcomes in patients treated with PBM, confirming its neutrality with respect to cancer responsiveness is a critical priority. Conclusion Based on its therapeutic effects, PBM may have utility in a broad range of oral, oropharyngeal, facial, and neck complications of HNC treatment. Although evidence suggests that PBM using LLLT is safe in HNC patients, more research is imperative and vigilance remains warranted to detect any potential adverse effects of PBM on cancer treatment outcomes and survival.

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Section: Pbm Effects On Tumor Cell Linesmentioning

confidence: 99%

Low level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 1: mechanisms of action, dosimetric, and safety considerations

Zecha

Raber-Durlacher

Nair

et al. 2016

Support Care Cancer

208

140

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“…Under the right irradiation conditions cell growth inhibition has been reported. Under long irradiation times the growth and proliferation of a human glioblastoma cell line was significantly inhibited [148]. Studies led by Fonseca have found evidence of genetic damage [149], increased mRNA and protein expression involved in DNA repair and genomic stabilization [150], and increasing occurrence of both apoptosis and necrosis [151] in white blood cells and myoblasts exposed to 808 nm light.…”

Section: Direct Optical Excitation Of 1o2mentioning

confidence: 99%

Direct 1O2 optical excitation: A tool for redox biology

Blázquez‐Castro

2017

Redox Biology

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Molecular oxygen (O2) displays very interesting properties. Its first excited state, commonly known as singlet oxygen (1O2), is one of the so-called Reactive Oxygen Species (ROS). It has been implicated in many redox processes in biological systems. For many decades its role has been that of a deleterious chemical species, although very positive clinical applications in the Photodynamic Therapy of cancer (PDT) have been reported. More recently, many ROS, and also 1O2, are in the spotlight because of their role in physiological signaling, like cell proliferation or tissue regeneration. However, there are methodological shortcomings to properly assess the role of 1O2 in redox biology with classical generation procedures. In this review the direct optical excitation of O2 to produce 1O2 will be introduced, in order to present its main advantages and drawbacks for biological studies. This photonic approach can provide with many interesting possibilities to understand and put to use ROS in redox signaling and in the biomedical field.

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“…dose-dependent manner (25). Frigo et al reported that 660-nm LPLI at 21 J/cm 2 negatively affected 3T3 murine fibroblast cells, as it increased cell death and inhibited cell proliferation (9).…”

Section: Innovationmentioning

confidence: 99%

Cancer PhototherapyviaSelective Photoinactivation of Respiratory Chain Oxidase to Trigger a Fatal Superoxide Anion Burst

Zhou

Wei

et al. 2014

Antioxidants & Redox Signaling

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Aims: Here, we develop a novel cancer treatment modality using mitochondria-targeting, high-fluence, lowpower laser irradiation (HF-LPLI) in mouse tumor models and explore the mechanism of mitochondrial injury by HF-LPLI. Results: We demonstrated that the initial reaction after photon absorption was photosensitization of cytochrome c oxidase (COX), to inhibit enzymatic activity of COX in situ and cause respiratory chain superoxide anion (O 2 -) burst. We also found that HF-LPLI exerted its main tumor killing effect through mitochondrial O 2 -burst via electron transport chain (ETC). These phenomena were completely absent in the respiration-deficient cells and COX knockdown cells. With a carefully selected irradiation protocol, HF-LPLI could efficaciously destroy tumors. The inhibition of enzymatic activity of COX and generation of O 2 -by HF-LPLI in vivo were also detected. Innovation: It is the first time that the mechanism involved in the interaction between light and its photoacceptor under HF-LPLI treatment is clarified. Our results clearly indicate that HF-LPLI initiates its effects via targeted COX photoinactivation and that the tumor-killing efficacy is dependent of the subsequent mitochondrial O 2 -burst via ETC. Conclusion: Based on both in vitro and in vivo results, we conclude that HF-LPLI can selectively photoinactivate respiratory chain oxidase to trigger a fatal mitochondrial O 2 -burst, producing oxidative damage on cancer cells. This study opens up the possibilities of applications of HF-LPLI as a mitochondria-targeting cancer phototherapy. Antioxid. Redox Signal. 20,[733][734][735][736][737][738][739][740][741][742][743][744][745][746]

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Low-power 808-nm laser irradiation inhibits cell proliferation of a human-derived glioblastoma cell line in vitro

Cited by 43 publications

References 31 publications

Low level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 1: mechanisms of action, dosimetric, and safety considerations

Low level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 1: mechanisms of action, dosimetric, and safety considerations

Direct 1O2 optical excitation: A tool for redox biology

Cancer PhototherapyviaSelective Photoinactivation of Respiratory Chain Oxidase to Trigger a Fatal Superoxide Anion Burst

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