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Shidai Jin
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P2.13 - Targeted Therapy (Not CME Accredited Session) (ID 962)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.13-29 - IL-22 Confers Resistance To EGFR-TKIs In Non-Small Cell Lung Cancer Bearing EGFR Gene Mutation and Amplification (ID 11857)
16:45 - 18:00 | Author(s): Shidai Jin
- Abstract
Background
The effect of epidermal growth factor receptor(EGFR)-targeted strategy is hindered by drug resistance. IL-22 can promote tumor growth and induce resistance to chemotherapy in human lung cancer cells. The aim of our study was to investigate the mechanism of IL-22-induced resistance to EGFR-tyrosine kinase inhibitors(EGFR-TKIs)in the NSCLC.
a9ded1e5ce5d75814730bb4caaf49419 Method
The tissues and plasma of patients taking EGFR-TKIs were used to examine the correlation between the drug’s efficacy and IL-22 level. We identified IL-22-induced EGFR-TKIs resistance and the effect of IL-22 on EGFR/AKT/ERK pathways in NSCLC PC-9 and HCC827 cells by CCK-8 assay, flow cytometric analysis, and western blotting. Then, we established the PC-9 xenograft model with IL-22 exposure and used gefitinib combined with vehicle or IL-22 to treat mice.
4c3880bb027f159e801041b1021e88e8 Result
We confirmed that IL-22 can inhibit the effect of gefitinib on NSCLC cells and determined the effects of IL-22 on EGFR/AKT/ERK pathways. Then, we showed that IL-22 exposures could promote tumor growth and induce resistance to gefitinib in the PC-9 xenograft model.
8eea62084ca7e541d918e823422bd82e Conclusion
These results suggest that IL-22 contributes to tumor progression and EGFR-TKIs resistance in NSCLC. Therefore, IL-22 is a potential therapeutic target for EGFR-TKIs resistance.
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