Epigallocatechin Gallate Enhances MAL-PDT Cytotoxic Effect on PDT-Resistant Skin Cancer Squamous Cells

Int J Mol Sci. 2020 May 8;21(9):3327. doi: 10.3390/ijms21093327.

Abstract

Photodynamic therapy (PDT) has been used to treat certain types of non-melanoma skin cancer with promising results. However, some skin lesions have not fully responded to this treatment, suggesting a potential PDT-resistant phenotype. Therefore, novel therapeutic alternatives must be identified that improve PDT in resistant skin cancer. In this study, we analyzed the cell viability, intracellular protoporphyrin IX (PpIX) content and subcellular localization, proliferation profile, cell death, reactive oxygen species (ROS) detection and relative gene expression in PDT-resistant HSC-1 cells. PDT-resistant HSC-1 cells show a low quantity of protoporphyrin IX and low levels of ROS, and thus a low rate of death cell. Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes. On the other hand, epigallocatechin gallate catechin enhanced the MAL-PDT effect, increasing levels of protoporphyrin IX and ROS, and killing 100% of resistant cells. The resistant MAL-PDT model of skin cancer squamous cells (HSC-1) is a reliable and useful tool to understand PDT cytotoxicity and cellular response. These resistant cells were successfully sensitized with epigallocatechin gallate catechin. The in vitro epigallocatechin gallate catechin effect as an enhancer of MAL-PDT in resistant cells is promising in the treatment of difficult skin cancer lesions.

Keywords: methyl aminolevulinate; non-melanoma skin cancer; photodynamic therapy; squamous cell carcinoma.

MeSH terms

  • Aminolevulinic Acid / analogs & derivatives
  • Aminolevulinic Acid / pharmacology
  • Anticarcinogenic Agents / pharmacology*
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / radiotherapy
  • Catechin / analogs & derivatives*
  • Catechin / pharmacology
  • Cell Death / drug effects*
  • Cell Death / radiation effects
  • Cell Hypoxia / drug effects
  • Cell Hypoxia / genetics
  • Cell Hypoxia / radiation effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cell Proliferation / radiation effects
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Combined Modality Therapy / methods*
  • Ferrochelatase / genetics
  • Ferrochelatase / metabolism
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism
  • Humans
  • Membrane Transport Proteins / genetics
  • Membrane Transport Proteins / metabolism
  • Molecular Chaperones / genetics
  • Molecular Chaperones / metabolism
  • Photochemotherapy / methods*
  • Photosensitizing Agents / metabolism
  • Protoporphyrins / metabolism
  • Reactive Oxygen Species / metabolism
  • Skin Neoplasms / drug therapy*
  • Skin Neoplasms / radiotherapy
  • Stress, Physiological / drug effects
  • Stress, Physiological / genetics
  • Stress, Physiological / radiation effects
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Survivin / genetics
  • Survivin / metabolism
  • Symporters / genetics
  • Symporters / metabolism

Substances

  • Anticarcinogenic Agents
  • BIRC5 protein, human
  • HSPB1 protein, human
  • Heat-Shock Proteins
  • Membrane Transport Proteins
  • Molecular Chaperones
  • Photosensitizing Agents
  • Protoporphyrins
  • Reactive Oxygen Species
  • Survivin
  • Symporters
  • hydrogen-coupled oligopeptide transporter PepT2
  • methyl 5-aminolevulinate
  • Aminolevulinic Acid
  • Catechin
  • epigallocatechin gallate
  • protoporphyrin IX
  • Superoxide Dismutase
  • superoxide dismutase 2
  • FECH protein, human
  • Ferrochelatase