TRIM24介导肺癌细胞吉非替尼耐药机制探讨

BACKGROUND AND OBJECTIVE: Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance signifcantly limits its use in clinical practice. Study found that TRIM24 was overexpressed in non-small cell lung cancer (NSCLC) tissues and regulate cell growth, cell cycle and apoptosis in lung cell lines. Te aim of this study is to explore the mechanism of TRIM24 to regulate resistance of Geftinib in NSCLC cells. METHODS: MTT and apoptosis were used to detect the change of cell grow and cell apoptosis with down-expression TRIM24 and ShTRIM24 with presence of Geftinib. Meanwhile, Western blot was used to detect the expression of protein related to apoptosis and AKT signal path. RESULTS: TRIM24 interference could improve the effect of gefitinib on cell growth inhibition and upregulate the cell apoptosis in A549 cell. Down-regulated of endogenous TRIM24 and ShTRIM24 with Giftinib could also reduce the protein related apoptosis, such as p-BAD and Bcl-2, and the protein PIK3CA related AKT signal path in A549 cell. CONCLUSION: TRIM24 could regulate required resistance to Geftinib via Akt pathway in NSCLC.