Low-level laser therapy can produce increased aggressiveness of dysplastic and oral cancer cell lines by modulation of Akt/mTOR signaling pathway

Authors

  • Felipe F. Sperandio,

    Corresponding author
    1. Department of Oral Pathology, School of Dentistry, University of São Paulo, 2227 Prof. Lineu Prestes Av., Cidade Universitária, S∼ao Paulo, SP Brazil 05508-000, Brazil
    2. The Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA, USA
    3. Department of Dermatology, Harvard Medical School, Boston, MA, USA
    • Phone: +55 11 30917984, Fax: 30917902
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  • Fernanda S. Giudice,

    1. Department of Oral Pathology, School of Dentistry, University of São Paulo, 2227 Prof. Lineu Prestes Av., Cidade Universitária, S∼ao Paulo, SP Brazil 05508-000, Brazil
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  • Luciana Corrêa,

    1. Department of Oral Pathology, School of Dentistry, University of São Paulo, 2227 Prof. Lineu Prestes Av., Cidade Universitária, S∼ao Paulo, SP Brazil 05508-000, Brazil
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  • Décio S. Pinto Jr.,

    1. Department of Oral Pathology, School of Dentistry, University of São Paulo, 2227 Prof. Lineu Prestes Av., Cidade Universitária, S∼ao Paulo, SP Brazil 05508-000, Brazil
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  • Michael R. Hamblin,

    1. The Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA, USA
    2. Department of Dermatology, Harvard Medical School, Boston, MA, USA
    3. Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA, USA
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  • Suzana C.O.M. de Sousa

    1. Department of Oral Pathology, School of Dentistry, University of São Paulo, 2227 Prof. Lineu Prestes Av., Cidade Universitária, S∼ao Paulo, SP Brazil 05508-000, Brazil
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Abstract

Low-level laser therapy (LLLT) is a non-thermal phototherapy used in several medical applications, including wound healing, reduction of pain and amelioration of oral mucositis. Nevertheless, the effects of LLLT upon cancer or dysplastic cells have been so far poorly studied. Head and neck cancer patients receiving LLLT for oral mucositis, for example, might have remaining tumor cells that could be stimulated by LLLT. This study demonstrated that LLLT (GaAlAs – 660 nm or 780 nm, 40 mW, 2.05, 3.07 or 6.15 J/cm2) can modify oral dysplastic cells (DOK) and oral cancer cells (SCC9 and SCC25) growth by modulating the Akt/mTOR/CyclinD1 signaling pathway; LLLT significantly modified the expression of proteins related to progression and invasion in all the cell lines, and could aggravate oral cancer cellular behavior, increasing the expression of pAkt, pS6 and Cyclin D1 proteins and producing an aggressive Hsp90 isoform. Apoptosis was detected for SCC25 and was related to pAkt levels. (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

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