EGCG’s anticancer potential unveiled: triggering apoptosis in lung cancer cell lines through in vitro investigation

• Published in: PeerJ (San Francisco, CA) Vol. 13; p. e19135
• Main Authors: Khair, Al Moutassem Billah, Maniangat Luke, Alexander, Patnaik, Rajashree, Testarelli, Luca
• Format: Journal Article
• Language: English
• Published: United States PeerJ. Ltd 26.03.2025; PeerJ, Inc; PeerJ Inc
• Subjects: 1-Phosphatidylinositol 3-kinase; A549 Cells; AKT protein; Anticancer properties; Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Apoptosis rate; Breast cancer; Cancer; Cancer therapies; Care and treatment; Catechin; Catechin - analogs & derivatives; Catechin - pharmacology; Cell Biology; Cell cycle; Cell growth; Cell Line, Tumor; Cell Movement - drug effects; Cell proliferation; Cell Proliferation - drug effects; Drug therapy; Epidermal growth factor; Epigallocatechin -3- gallate (EGCG); Epigallocatechin gallate; Green tea; H1299 cell; Human subjects; Humans; Investigations; Kinases; Lung cancer; Lung Neoplasms - drug therapy; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Medical research; Molecular Biology; Oncology; Pharmacology; Phosphatidylinositol; Phosphatidylinositol 3-Kinases - metabolism; Protein kinases; Proteins; Proto-Oncogene Proteins c-akt - metabolism; Respiratory agents; Respiratory Medicine; Signal transduction; Signal Transduction - drug effects; Tumor cell lines; Massachusetts; United States > US; India; Cell proliferation; A549 cells; Lung cancer; Apoptosis rate; Protein expression; Epigallocatechin -3- gallate (EGCG); H1299 cell
• ISSN: 2167-8359; 2167-8359; 2376-5992
• DOI: 10.7717/peerj.19135

Novel treatment techniques are needed since lung cancer is still a major worldwide health concern. Green tea contains a component called epigallocatechin-3-gallate (EGCG), which has demonstrated potential anticancer properties. This work sought to understand how EGCG affects the phosphatidylinositol-3-kinase protein kinase B (PI3K/Akt) signaling pathway, which in turn causes apoptosis in H1299 lung cancer cells. In this experiment, multiple dosages of EGCG were applied to five H1299 cells and five A549 cell lines for a duration of 72 h. Apoptotic pathways, cellular responses, and protein expression levels were investigated in relation to EGCG by morphological, biochemical, and proliferation/migration investigations. In H1299 and A549 cells, EGCG raised apoptosis rates and, in a dose-dependent way, hindered cell growth. The levels of phosphorylated Akt (p-Akt) and PI3K (p-PI3K) dramatically reduced following EGCG administration, despite no significant alterations in Akt and PI3K expressions. These results imply that EGCG inhibits the activation of the PI3K/Akt signaling pathway, which in turn causes apoptosis in H1299 and A549 cells. The research provides insights into the effects of EGCG on proliferation and migratory inhibition, as well as highlighting its potential to induce apoptosis in lung cancer cells. These results support EGCG's promise as a therapeutic agent in the treatment of lung cancer and further our understanding of the processes underlying its anticancer activities.