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.
Highlights
Research findings suggest that a small heterogeneous subpopulation of cells is the origin of cancer development [1]
This study proves that Photodynamic therapy (PDT) using AlPcS4Cl has the desired effects of killing lung cancer stem cells (CSCs), where intracellular localization of the PS was seen to be in the cytosol and around integral organelles, where membrane permeabilization and disruption of cell homeostasis through increased free radical production lead to cellular destruction
AlPcS4Cl-PDT further proved to be effective in causing apoptotic lung CSC death by inducing significant mitochondrial damage shown by a decrease in Δψm, upon photoactivation of the PS causing eradication of the cells through apoptotic cell death
Summary
Research findings suggest that a small heterogeneous subpopulation of cells is the origin of cancer development [1]. Multi-differentiation potential, can metastasize [2] and are known to evade drug-induced cell death, 2 mainly due to their quiescent stem-like nature [3], where this state of dormancy is characterized as a recurrent clinical occurrence where diffuse tumour cells are retained in a non-proliferating quiescent state for long periods of time This phenomenon can occur at an early stage of the disease or after a therapeutic intervention. Self-conservation of CSCs is allowed by asymmetrical cell division cycles, where the CSC population is retained resulting in a heterogeneous tumour population of CSCs and non-stem-like cancer cells [6] These non-stem-like cancer cells undergo rapid symmetrical cell proliferation, making them susceptible to conventional cancer treatment and preserving the CSC population, justifying treatment failure and cancer relapse [7]. CSCs demonstrate high drug resistance and resilience due to extended telomere duration, initiation toward apoptotic pathways, increased membrane transporter activity and their ability to travel and metastasize [8]
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