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Background <p>Photobiomodulation (PBM) therapy, utilizing light to regulate cellular processes, holds promise as a cancer treatment. We aimed to explore PBM's impact on two oral squamous cell carcinoma (OSCC) cell lines, Cal-27 and SCC-25, under varying blue light irradiation conditions.</p> Methods <p>Cal-27 and SCC-25 cells were exposed to 457&#xa0;nm blue light at varying irradiances (2.5–70&#xa0;mW/cm<sup>2</sup>) and radiant exposure levels (3–84&#xa0;J/cm<sup>2</sup>). Cell viability, reactive oxygen species levels, mitochondrial function, apoptosis, proliferation, and proteins related to proliferation and autophagy were quantified.</p> Results <p>457&#xa0;nm blue light significantly reduced OSCC cell viability, with efficacy increasing proportionally to radiant exposure. This effect resulted primarily from inhibited cell proliferation, as we observed no significant apoptosis or necrosis. Additionally, blue light elevated reactive oxygen species levels in OSCC cells while selectively decreasing mitochondrial membrane potential in SCC-25 cells, suggesting variable cell-type responses. Besides, autophagy levels were modulated by blue light exposure.</p> Conclusion <p>The study demonstrates that 457&#xa0;nm blue LED photobiomodulation therapy inhibits OSCC cell progression by promoting autophagy and inhibiting PI3K/AKT pathway-mediated cell proliferation. These insights provide a basis for exploring therapeutic applications of photobiomodulation in oral cancer treatment.</p> Graphical Abstract <p></p>

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457 nm LED blue light inhibits oral squamous cell carcinoma cell proliferation via the PI3K/AKT pathway and autophagy

  • 期刊论文

  • 发表日期：

    2025年6月18日

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  • Hui Jiang,
  • Jiali Yang,
  • Qiqi Fu,
  • Haokuan Qin,
  • Muqing Liu

摘要

Background

Photobiomodulation (PBM) therapy, utilizing light to regulate cellular processes, holds promise as a cancer treatment. We aimed to explore PBM's impact on two oral squamous cell carcinoma (OSCC) cell lines, Cal-27 and SCC-25, under varying blue light irradiation conditions.

Methods

Cal-27 and SCC-25 cells were exposed to 457 nm blue light at varying irradiances (2.5–70 mW/cm2) and radiant exposure levels (3–84 J/cm2). Cell viability, reactive oxygen species levels, mitochondrial function, apoptosis, proliferation, and proteins related to proliferation and autophagy were quantified.

Results

457 nm blue light significantly reduced OSCC cell viability, with efficacy increasing proportionally to radiant exposure. This effect resulted primarily from inhibited cell proliferation, as we observed no significant apoptosis or necrosis. Additionally, blue light elevated reactive oxygen species levels in OSCC cells while selectively decreasing mitochondrial membrane potential in SCC-25 cells, suggesting variable cell-type responses. Besides, autophagy levels were modulated by blue light exposure.

Conclusion

The study demonstrates that 457 nm blue LED photobiomodulation therapy inhibits OSCC cell progression by promoting autophagy and inhibiting PI3K/AKT pathway-mediated cell proliferation. These insights provide a basis for exploring therapeutic applications of photobiomodulation in oral cancer treatment.

Graphical Abstract