Journal, genetic engineering & biotechnology · 2026
Evaluation of phloroglucinol for cytotoxic and anti-inflammatory effects in lung adenocarcinoma cells.
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Karuppan Perumal Manoj Kumar, Hirad Abdurahman Hajinur, Choi Ki Choon, Dharmalingam Jothinathan Mukesh Kumar, Rajan Renuka Remya
Аннотация
BACKGROUND AND OBJECTIVE: Phloroglucinol (PGL) is a polyphenol which is present in marine brown algae and has been reported to exhibit antioxidant and immunomodulatory properties. However, its anticancer potential remains largely unexplored. This research examined the cytotoxic, apoptotic, and anti-inflammatory properties of PGL in A549 cell lines, highlighting its potential for repurposing in cancer treatment.
METHODS AND MATERIALS: A549 cells were treated with varying concentrations of PGL for different time intervals. Cell viability was assessed by MTT assay, morphological changes by microscopy, and cell cycle progression and apoptosis by flow cytometry. Nuclear condensation and intracellular ROS generation were analyzed using DAPI and DCF-DA staining. Cell migration was examined using a wound healing assay, and transcriptional changes in pro-inflammatory cytokines were quantified by RT-qPCR.
RESULTS: PGL caused dose- and time-dependent cytotoxicity in A549 cells, and the values of IC50 dropped to 80 μM after 24 h to about 40 μM after 72 h. The apoptotic characteristics were observed in treated cells such as membrane blebbing, shrinkage, and detachment. Flow cytometry showed G0/G1 arrest (82.10%) and late apoptosis (17.89%). Nuclear condensation and increased ROS production were observed by DAPI and DCF-DA staining. PGL also blocked cell migration of A549 cell and suppressed the transcription of pro-inflammatory cytokines.
CONCLUSIONS: PGL induced dose and time-dependent cytotoxicity in A549 cells, with G0/G1 arrest, ROS-mediated apoptosis, reduced migration, and cytokine downregulation. Crucially, its lower toxicity in fibroblasts suggests selectivity in anticancer activity.
METHODS AND MATERIALS: A549 cells were treated with varying concentrations of PGL for different time intervals. Cell viability was assessed by MTT assay, morphological changes by microscopy, and cell cycle progression and apoptosis by flow cytometry. Nuclear condensation and intracellular ROS generation were analyzed using DAPI and DCF-DA staining. Cell migration was examined using a wound healing assay, and transcriptional changes in pro-inflammatory cytokines were quantified by RT-qPCR.
RESULTS: PGL caused dose- and time-dependent cytotoxicity in A549 cells, and the values of IC50 dropped to 80 μM after 24 h to about 40 μM after 72 h. The apoptotic characteristics were observed in treated cells such as membrane blebbing, shrinkage, and detachment. Flow cytometry showed G0/G1 arrest (82.10%) and late apoptosis (17.89%). Nuclear condensation and increased ROS production were observed by DAPI and DCF-DA staining. PGL also blocked cell migration of A549 cell and suppressed the transcription of pro-inflammatory cytokines.
CONCLUSIONS: PGL induced dose and time-dependent cytotoxicity in A549 cells, with G0/G1 arrest, ROS-mediated apoptosis, reduced migration, and cytokine downregulation. Crucially, its lower toxicity in fibroblasts suggests selectivity in anticancer activity.