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Aluminium (III) phthalocyanine chloride tetrasulphonate is an effective photosensitizer for the eradication of lung cancer stem cells.

ABSTRACT: Cancer stem cells (CSCs) are considered to contribute to the recurrence of lung cancer due to their stem-like nature and the involvement of genetic markers associated with drug efflux, regeneration and metastases. Photodynamic therapy (PDT) is a cost-effective and non-invasive therapeutic application that can act as an alternative therapy for lung cancer when considering CSC involvement. Stem-like cells derived from the A549 lung cancer cell line, positive for CD133, CD56 and CD44 antigen markers, were characterized, intracellular localization of aluminium (III) phthalocyanine chloride tetrasulphonate (AlPcS₄Cl) determined and its anti-cancer PDT effects were evaluated. Results confirmed that isolated cells were stem cell-like and subcellular localization of AlPcS₄Cl in integral organelles involved in cell homeostasis supported the destruction of CSC. AlPcS₄Cl's effectivity was demonstrated with CSC eradication showing a significant increase in cytotoxicity and cell death via apoptosis, caused by a decrease in mitochondrial membrane potential. PDT could serve as a palliative treatment for lung cancer and improve prognosis by elimination of lung CSCs.

SUBMITTER: Crous A

PROVIDER: S-EPMC8424323 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionPhotodynamic therapy (PDT) is a light-based technique used in the treatment of malignant and non-malignant tissue. Aluminium-phthalocyanine chloride tetra sulfonate (AlPcS4Cl)-mediated PDT has been well investigated on several cancer types, including oesophageal cancer. However, the effects of (AlPcS4Cl)-mediated PDT on DNA damage response and the mechanism of cell death in oesophageal cancer needs further investigation.MethodsHere, we examined the in vitro effects of AlPcS4Cl-mediated PDT on cell cycle, DNA damage response, oxidative stress, and intrinsic apoptotic cell death pathway in HKESC-1 oesophageal cancer cells. The HKESC-1 cells were exposed to PDT using a semiconductor laser diode (673.2 nm, 5 J/cm2 fluency). Cell viability and cytotoxicity were determined by the ATP cell viability assay and the lactate dehydrogenase (LDH) release assay, respectively. Cell cycle and DNA damage response (DDR) analyses were conducted using the Muse™ cell cycle kit and the Muse® multi-color DNA damage kit, respectively. The mode of cell death was identified using the Annexin V-FITC/PI detection assay and Muse® Autophagy LC3 antibody-based kit. The intrinsic apoptotic pathway was investigated by measuring the cellular reactive oxygen species (ROS) levels, mitochondrial membrane potential (ΔΨm) function, cytochrome c levels and the activity of caspase 3/7 enzymes.ResultsThe results show that AlPcS4Cl-based PDT reduced cell viability, induced cytotoxicity, cell cycle arrest at the G0/G1 phase, and DNA double-strand break (DSB) through the upregulation of the ataxia telangiectasia mutated (ATM), a DNA damage sensor. In addition, the findings showed that AlPcS4Cl-based PDT induced cell death via apoptosis, which is observed through increased ROS production, reduced ΔΨm, increased cytochrome c release, and activation of caspase 3/7 enzyme. Finally, no autophagy was observed in the AlPcS4Cl-mediated PDT-treated cells.ConclusionOur findings showed that apoptotic cell death is the main cell death mechanism triggered by AlPcS4Cl-mediated PDT in oesophageal cancer cells.

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Aluminium (III) phthalocyanine chloride tetrasulphonate is an effective photosensitizer for the eradication of lung cancer stem cells.

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