Fig. 7
From: Angiopoietin-like protein 3 blocks nuclear import of FAK and contributes to sorafenib response
High ANGPTL3 levels predict better responses to sorafenib in RCC patients. a, b Kaplan–Meier analysis of PFS in RCC patients with and without sorafenib therapy. a All patients regardless of ANGPTL3 expression (p = 0.010). b patients with high levels (left, p = 0.0084) or low levels (right, p = 0.261) of ANGPTL3 expression. c Immunostaining of ANGPTL3, FAK and p53 in consecutive tumour sections from matched human RCC taken before sorafenib therapy (Pre-therapy) and after sorafenib resistance (Post-relapse). Black scale bar represents 50 μm. Micrograph indicates the magnified morphology of tumour tissue.Blue scale bar represents 10 μm. d Schematic diagram of the ANGPTL3-based signalling pathway in RCC sorafenib sensitivity. FAK enters the nucleus under sorafenib treatment and leads to ubiquitination of p53, thereby inhibiting cellular apoptosis; ANGPTL3 can reverse this process by binding to FAK and inhibiting its nuclear localisation. See also See also Supplementary Figure 7 and Supplementary Table 5-7
