Fig. 7

Phosphorylation of STYK1 at Y191 by BLK kinase enhances pancreatic cancer cell proliferation. a Co-IP/Western blot analysis of Flag-STYK1 interactions with TEC/SRC kinase subfamily members in HEK293T cells. b, c Co-IP/Western blot analysis of Flag-STYK1 interactions with HA-tagged BLK mutants in HEK293T cells, with corresponding domain mapping diagrams. d GST-STYK1 ICD and HA-BLK kinase reactions (with or without ATP) were analyzed by Western blot using HEK293T lysates. e Phosphorylation status of WT STYK1 and Y191F/Y356F mutants in BLK-expressing HEK293T cells was assessed via Western blot. f Tyrosine phosphorylation levels of Flag-STYK1 and Y191F mutant in BLK-overexpressing HEK293T cells with or without saracatinib treatment were assessed by IP-Western. g GST-STYK1 ICD (WT/Y191F) and HA-BLK kinase reactions (with or without saracatinib/ATP) were analyzed by Western blot using HEK293T lysates. h Total phosphorylation levels of wild-type STYK1 upon BLK, its continuous-activated and kinase-dead mutants transfection in HEK293T cells were analyzed using western blot assay. i Schematic and representative images of PANC-1 xenograft tumors (Flag-STYK1 WT/Y191F/Y191D/SS123 mutants) with XAV939/CQ treatment timepoints. j Tumor growth kinetics post-injection (n = 3). k Excised tumor weights. l H&E and IHC staining (Ki67/Axin2/CyclinD1/p62) in tumor tissues (n = 3). Data were represented as mean ± SD, *p < 0.05; **p < 0.01; ***p < 0.001