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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: FLI1 regulates radiotherapy resistance in nasopharyngeal carcinoma through TIE1-mediated PI3K/AKT signaling pathway

Fig. 5

Source data are provided as a Source Data file

FLI1 regulates TIE1-mediated PI3K/AKT signaling pathway in NPC cells. A KEGG pathway analysis of genes regulated by FLI1 in CNE1 and 5-8F cells. PI3K/AKT pathway was among the significant pathways. B Western blot analysis of TIE1, PI3K, p-PI3K, AKT, p-AKT (Thr308) and p-AKT (Ser473) in CNE1 cells with FLI1 overexpression and 5-8F cells with FLI1 knockdown. C CNE1-VEC and CNE1-FLI1 cells were transiently transfected with siTIE1 or control siRNA. 5-8F-NC and 5-8F-shFLI1 cells were transiently transfected with TIE1 or empty vector plasmids. Western blot assays were performed to assess the protein level of TIE1, PI3K, p-PI3K, AKT, p-AKT (Thr308) and p-AKT (Ser473). D–E CNE1-VEC and CNE1-FLI1 cells were treated with IR, a PI3K inhibitor BKM120 (3 μM) and an AKT inhibitor MK2206 (3 μM). Colony formation assays and survival fraction curve analysis D were employed to assess cell survival at 10–14 days after exposure to indicated IR dose. Cell apoptosis E was determined by Annexin V/PI double-staining assays at 48 h after indicated treatment. Data in D and E are presented as mean ± SD (n = 3). **p < 0.01; ns, not significant (Student’s t-test).

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