Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells

Photobiomodulation (PBM) therapy is a relatively new modality for the combined treatment of cancer. Pre-treatment of certain types of cancer cells with PBM potentiates the treatment efficacy of photodynamic therapy (PDT). The mechanism of action of this synergetic effect is not yet fully understood....

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Main Authors: Viktória Pevná, Georges Wagnières, Daniel Jancura, Veronika Huntošová
Format: Article
Language:English
Published: MDPI AG 2023-05-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/12/10/1441
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author Viktória Pevná
Georges Wagnières
Daniel Jancura
Veronika Huntošová
author_facet Viktória Pevná
Georges Wagnières
Daniel Jancura
Veronika Huntošová
author_sort Viktória Pevná
collection DOAJ
description Photobiomodulation (PBM) therapy is a relatively new modality for the combined treatment of cancer. Pre-treatment of certain types of cancer cells with PBM potentiates the treatment efficacy of photodynamic therapy (PDT). The mechanism of action of this synergetic effect is not yet fully understood. In the present study, we focused on protein kinase Cδ (PKCδ) as a proapoptotic agent that is highly expressed in U87MG cells. The distribution of PKCδ in the cytoplasm was changed and its concentration was increased by PBM using radiation at 808 nm (15 mW/cm<sup>2</sup>, 120 s). This process was accompanied by the organelle specific phosphorylation of PKCδ amino acids (serine/tyrosine). Enhanced phosphorylation of serine 645 in the catalytic domain of PKCδ was found in the cytoplasm, whereas the phosphorylation of tyrosine 311 was mainly localized in the mitochondria. Despite a local increase in the level of oxidative stress, only a small amount of cytochrome c was released from the mitochondria to cytosol. Although a partial inhibition of mitochondrial metabolic activity was induced in PBM-exposed cells, apoptosis was not observed. We hypothesized that PBM-induced photodamage of organelles was neutralized by autophagy maintained in these cells. However, photodynamic therapy may effectively exploit this behaviour to generate apoptosis in cancer treatment, which may increase the treatment efficacy and open up prospects for further applications.
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spelling doaj.art-ccaacfe87ff547c382de6d1123a08cb72023-11-18T00:53:39ZengMDPI AGCells2073-44092023-05-011210144110.3390/cells12101441Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG CellsViktória Pevná0Georges Wagnières1Daniel Jancura2Veronika Huntošová3Department of Biophysics, Institute of Physics, Faculty of Science, P.J. Safarik University in Kosice, Jesenna 5, 041 54 Kosice, SlovakiaLaboratory for Functional and Metabolic Imaging, Institute of Physics, Swiss Federal Institute of Technology in Lausanne (EPFL), Station 3, Building PH, 1015 Lausanne, SwitzerlandDepartment of Biophysics, Institute of Physics, Faculty of Science, P.J. Safarik University in Kosice, Jesenna 5, 041 54 Kosice, SlovakiaCenter for Interdisciplinary Biosciences, Technology and Innovation Park, P.J. Safarik University in Kosice, Jesenna 5, 041 54 Kosice, SlovakiaPhotobiomodulation (PBM) therapy is a relatively new modality for the combined treatment of cancer. Pre-treatment of certain types of cancer cells with PBM potentiates the treatment efficacy of photodynamic therapy (PDT). The mechanism of action of this synergetic effect is not yet fully understood. In the present study, we focused on protein kinase Cδ (PKCδ) as a proapoptotic agent that is highly expressed in U87MG cells. The distribution of PKCδ in the cytoplasm was changed and its concentration was increased by PBM using radiation at 808 nm (15 mW/cm<sup>2</sup>, 120 s). This process was accompanied by the organelle specific phosphorylation of PKCδ amino acids (serine/tyrosine). Enhanced phosphorylation of serine 645 in the catalytic domain of PKCδ was found in the cytoplasm, whereas the phosphorylation of tyrosine 311 was mainly localized in the mitochondria. Despite a local increase in the level of oxidative stress, only a small amount of cytochrome c was released from the mitochondria to cytosol. Although a partial inhibition of mitochondrial metabolic activity was induced in PBM-exposed cells, apoptosis was not observed. We hypothesized that PBM-induced photodamage of organelles was neutralized by autophagy maintained in these cells. However, photodynamic therapy may effectively exploit this behaviour to generate apoptosis in cancer treatment, which may increase the treatment efficacy and open up prospects for further applications.https://www.mdpi.com/2073-4409/12/10/1441photobiomodulationmitochondriaprotein kinase Ccytochrome cautophagyglioblastoma
spellingShingle Viktória Pevná
Georges Wagnières
Daniel Jancura
Veronika Huntošová
Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
Cells
photobiomodulation
mitochondria
protein kinase C
cytochrome c
autophagy
glioblastoma
title Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
title_full Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
title_fullStr Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
title_full_unstemmed Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
title_short Effect of Photobiomodulation on Protein Kinase Cδ, Cytochrome C, and Mitochondria in U87 MG Cells
title_sort effect of photobiomodulation on protein kinase cδ cytochrome c and mitochondria in u87 mg cells
topic photobiomodulation
mitochondria
protein kinase C
cytochrome c
autophagy
glioblastoma
url https://www.mdpi.com/2073-4409/12/10/1441
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