Fig. 6

The role of predictive survival and tumorigenesis effects of PRTN3 in heat stress treated HCC. A Immunohistochemical analysis indicated that the expression of PRTN3 in HCC was increased after RFA. B-C Representative immunohistochemical images of PRTN3 expression in HCC tissues before the first RFA treatment (B) and before the second RFA treatment (C). D-E Kaplan‒Meier analysis showing the OS predictive abilities of PRTN3 before RFA treatment (D) and after RFA treatment (E) in patients with early recurrence of HCC. F Immunofluorescence staining of DAPI and CD68 in KCs. G-H Cell proliferation assay of Hep 3B and SMMC-7721 after heat stress treatments and cultured with KC-CM transfected by lentiviral vector for PRTN3-overexpression (PR3OE) or PRTN3-knockdown (PR3KD). I Wound-healing assay. J Cell migration and invasion assays by transwell. K Western blot analysis of protein expression levels of CXCL5, MPO, MMP9 and IL-6 in heat stress HCC cells as were affected by KC-CM after PR3OE or PR3KD. L Western blot analysis of protein expression of p-AKT, p-ERK1/2, p-P38 and PI3K in heat stress HCC cells affected by KC-CM after PR3OE or PR3KD. M Picture of xenograft tumors were shown in the PR3OE group and wild type group (n = 5). N: The growth curves of each group of xenograft tumors were displayed. O The xenograft mice models in vivo were analyzed by IVIS to identify the potential of PRTN3 in promoting tumor grow. All data are expressed as the mean ± SD of three independent experiments. **p < 0.01