Fig. 4

Caprin-1 interacts with ULK1 and STK38 that activates autophagy and drives tumor growth. A The autophagy flux was tracking by tandem fluorescent-tagged LC3 (mRFP-EGFP-LC3) assay in Panc-1 cells. B, C The expressions of autophagy genes LC3, p62, ULK1 and p-ULK1 were detected in cancer cells with knockdown or overexpression of Caprin-1. D The autophagy gene LC3B was stained in orthotopic tumors using IHC staining. E, F Co-IP assay validated the interaction between Caprin-1 and ULK1 in both Bxpc-3 and Panc-1 cell lines. G The level of ULK1 was tested in tumor microarray by IHC staining. H The Kaplan–Meier analysis compared the prognosis of patients with high and low expressed ULK1 in PDAC tissues. I The peptides interacted with Caprin-1 proteins were investigated by mass spectrometry and targeted proteins were predicted. J STK38 was predicted to bind with Caprin-1 in tumor cells. K, L The interaction between Caprin-1 and STK38 was certified by Co-IP assay. M The expressions of Caprin-1, STK38, ULK1 and p-ULK1 were examined in negative control, sh-Caprin-1, sh-STK38 and sh-Caprin-1 plus sh-STK38 groups in both Bxpc-3 and Panc-1 cells. N Kaplan–Meier curve plotted the overall survival of patients with high and low level of STK38 in PDAC