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Fig. 3 | Cell & Bioscience

Fig. 3

From: The two-faced role of ATF2 on cisplatin response in gastric cancer depends on p53 context

Fig. 3

The genetic status of p53 affects the function of ATF2. A STRING database analysis was performed to explore potential interactions between ATF2 and p53, then the overlapped genes was predicted with Venny software, and the KEGG pathway enrichment of sharing genes were further analyzed with STRING, top 5 pathways were shown. B Protein expression of p53 in GC cells after cisplatin treatment for 24 or 48 h was analyzed by Western Blot assay. C Protein expression of p53 in GC cell lines treated with different doses of cisplatin was analyzed by Western Blot. D The phosphorylation of p53 in cisplatin treating MGC-803 and AGS were detected with Western Blot. E HCT116 p53+/+ or HCT-116 p53−/− cells that over-expressing different ATF2 subtypes (WT, T71A, T71E) were treated with cisplatin, then p53, ATF2 and p-ATF2 (phospho-Thr71) level were detected by Western Blot. ATF2 wild type (ATF2-WT), inactivated mutant type that mutated Thr to Ala (ATF2-T71A), activated mutant type that mutated Thr to Glu (ATF2-T71E). F Cell proliferation and cytotoxicity of cisplatin treated ATF2 subtype colorectal cancer cell lines with incucyte live cell analysis system. Cisplatin was used at a final concentration of 2 µg/ml

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