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. 2021 Sep 25;12(10):878. doi: 10.1038/s41419-021-04118-4

Fig. 1. Aberrant HAT1 expression promotes gemcitabine resistance in pancreatic cancer cells.

Fig. 1

a MTS assay was used to detect the viability of PANC-1 after treating with different drugs. GraphPad Prism 7.0 software was used to calculate IC50. b MTS assay detected the viability of PANC-1 cells with normal, knockdown, and overexpressing HAT1 after treatment with gemcitabine. The cell viability curve showed IC50 values of gemcitabine among different groups. c–f PANC-1 cells were infected with lentivirus expressing control or HAT1-specific shRNAs. After infecting 72 h, cells were harvested and treated with gemcitabine (50 nM) for MTS assay (c), colony formation assay (d), cleaved caspase-3 activity assay (e), and Annexin-V/Propidium Iodide assay (f). All data were shown as mean values ± SD (n = 3). **P < 0.01; ***P < 0.001. gj PANC-1 cells were transfected with indicated plasmids for 72 h. Cell were subcutanousely injected into the nude mice. These mice were injected intraperitoneally with or without gemcitabine (10 mg/kg) every 3 days when tumor volume reached to 50 mm3. The tumor volume was measured every 3 days and all tumors were harvested for photograph and weight after 30 days (g–i). All tumors were conducted caspase-3 and Ki67 analysis by IHC staining (j). Data presented as Means ± SD (n = 5). ***P < 0.001.