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Fig. 7 | Journal of Translational Medicine

Fig. 7

From: Metabolic reprogramming based on RNA sequencing of gemcitabine-resistant cells reveals the FASN gene as a therapeutic for bladder cancer

Fig. 7

Upregulation of FASN promotes drug resistance and poor prognosis in BLCA. A The lipid content of bladder cancer cells and gemcitabine-resistant cells was quantified by BODIPY staining corrected total cell fluorescence (CTCF). B The contents of free fatty acids (FFAs), triglycerides (TGs) and total cholesterol (T-CHO) were used as intracellular lipid indexes. C The expression of FASN in bladder cancer cells resistant to different concentrations of gemcitabine was detected by Western blotting (WB). Density measurement and statistical analysis. Representative images are shown. D The expression of FASN in gemcitabine-resistant bladder cancer cells after FASN knockdown was detected by WB. E, F Cell viability and sensitivity to gemcitabine under all conditions were determined by CCK-8 assay. G The tumorigenic ability of single cells under all conditions was determined by colony formation assay. H, I The lipid content of gemcitabine-resistant cells after FASN knockdown was quantitatively detected by BODIPY staining corrected total cell fluorescence (CTCF) and the contents of free fatty acids (FFAs), triglycerides (TGs) and total bilirubin (T-CHO). J, K, and L Mice with stable knockdown expression of T24-R xenografts were treated with vector control or gemcitabine (50 mg/kg. IP. QOD) for approximately 5 weeks. Tumor volumes were measured every 5 days (n = 5 per group). Tumors were weighed after resection. The graphs show the means ± SEMs. One-way ANOVA followed by Tukey’s multiple comparison test. α = 0.05; *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****p < 0.0001; ns, no significance

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