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J.J. Li
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P1.05 - Poster Session/ Prevention and Tobacco Control (ID 215)
- Event: WCLC 2015
- Type: Poster
- Track: Prevention and Tobacco Control
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.05-009 - EGCG Regulated Ku70 Acetylation for Apoptosis in Human Lung Cancer A549 Cells (ID 194)
09:30 - 17:00 | Author(s): J.J. Li
- Abstract
Background:
Lung cancer is one of the malignant tumors whose global incidence and mortality are very high. The chemoprevention has become an important prevention and control means of lung cancer except for giving up smoking and early detection. Research has showed the main component in green tea (-)-epigallocatechin-3-gallate (EGCG) is a potential chemopreventive agent for various tumors, especially lung cancer.
Methods:
The cells in each group were treated with different concentrations of EGCG for a certain time in the experiment. Two gene point mutation plasmid were constructed and transfected in A549 cells. Induction of apoptosis was examined using AnnexinV/Pl double staining flow cytometry. Western Blot detected the protein expressions of Bax, Bcl-xl and Caspase-3. Co-immunoprecipitation was used to detect the interaction of Ku70-Bax and acetylation status of Ku70. P<0.05 showed the difference had statistical significance.
Results:
Treatment of A549 cells with EGCG induced apoptosis with increasing expression of Bax and Caspase-3, but decreasing expression of Bcl-xl. EGCG could up-regulate K70 acetylation status of A549 cells，then down-regulate the interaction of Bax-Ku70 in the manner of concentration and time dependent. The apoptosis-promoting effect of EGCG on A549 cells was obviously weakened with the interaction of Bax-Ku70 strengthened and Caspase-3 (17KDa) expression declining after pCDNA3.1(+)-Ku70 plasmid and pCDNA3.1(+) -Ku70[539/542R] plasmid transfection.
Conclusion:
The authors induced apoptosis in human lung adenocarcinoma A549 cells after treatment with EGCG, and it was realized by interfering the interaction between Ku70 and Bax through regulating K70 acetylation. It verified that two loci K539 and K542 of Ku70 acetylation might play a crucial role in EGCG inducing apoptosis of A549 cells.
