Study of EGCG induced apoptosis in lung cancer cells by inhibiting PI3K/Akt signaling pathway

J.-J. Gu, K.-S. Qiao, P. Sun, P. Chen, Q. Li

Department of Pharmacy, The Fourth People’s Hospital of Zibo, Zibo, P.R. China. pq5071@163.com

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• Oncology

OBJECTIVE: To investigate the role of phosphatidylinositol-3-kinase protein kinase B (PI3K/Akt) signaling pathway in the apoptosis of H1299 lung cancer cells induced by epigallocatechin gallate (EGCG).

MATERIALS AND METHODS: H1299 lung cancer cells were treated with EGCG at a dose of 10 µM, 20 µM, and 40 µM, respectively. Cell culture was performed for 72 h and then: 1, cell proliferation was detected by MTT assay; 2, cell apoptosis rate was detected by flow cytometry; 3, expression of Caspase-3, Bax, and Bcl-2 was detected by Western blot; 4, expression of PI3K, p-PI3K, Akt, and p-Akt was detected by Western blot.

RESULTS: The proliferation of H1299 cells was significantly inhibited 72 h after treatment with different doses of EGCG, and cell apoptosis rate was significantly increased (p<0.05). Compared with those in the control group, expression of PI3K and Akt in the lung cancer cells H1299 after EGCG treatment showed no significant differences (p>0.05), while expression levels of p-PI3K and p-Akt were significantly reduced (p<0.05).

CONCLUSIONS: EGCG can inhibit the proliferation and induce apoptosis of H1299 lung cancer cells, and the effect is related to the inhibition of the activation of PI3K/Akt signaling pathway.

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