Fig 1: Elevated STAT3 phosphorylation in radio-resistant BCa cells is associated with an increase of tumor cell stemness. (A) Western blot analysis of pSTAT3Tyr705, pSTAT3Ser727, STAT3, MMP-2, MMP-9, KMT1A, GATA3 and JAK2, GAPDH served as a loading control. (B) Quantification of migration analysis of PBS-treated (Ctrl) and S3I201-treated BCa cells. (C) Quantification of invasion analysis of Ctrl and S3I201-treated BCa cells. (D) Quantification of tumorspheres formed by Ctrl and S3I201-treated BCa cells. S3I-201 was added to the culture to the final concentration of 50 µM. (E) Quantification of soft agar colony formation analysis of Ctrl and S3I201-treated BCa cells. The data are presented as the mean ± SEM of triplicate experiments. STAT3, signal transduction and transcription activator 3; BCa, bladder cancer; p-, phosphorylated; MMP, matrix metalloproteinase; KMT1A, suppressor of variegation 3–9 homolog 1; GATA3, GATA binding protein 3; JAK2, Janus kinase 2; Ctrl, control; R, radio-resistant cells.