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. 2020 Apr 8;9(4):911. doi: 10.3390/cells9040911

Figure 3.

Figure 3

FGFR1 and PARP1 co-occur and directly interact with each other at the expense of RAD51/H2AFX signaling and with adverse prognostic implications. (A) Co-occurrence and mutual exclusivity analysis of FGFR1, PARP1, ALDH1A1, ABCB1, RAD51, and H2AFX in the TCGA pancreatic adenocarcinoma cohort. (B) FGFR1-PARP1 gene expression correlation in the TCGA pancreatic adenocarcinoma cohort. (C) Schrödinger’s PyMOL molecular graphics system-generated molecular docking of PARP1 and FGFR1. (D) PANC-1 and SUIT-2 cells were subjected to immunoprecipitation (IP) with FGFR1 (upper) or PARP1 (lower) antibody followed by Western blotting analysis with the indicated antibodies, with IgG serving as the control. (E) Interaction of PARP1 with fibroblast growth factor receptor 1 (FGFR1). Coimmunolocalization assays of PARP1 and FGFR1 in the PANC1 cancer cell lines expressing wild-type PARP1 and FGFR1. Kaplan–Meier plots showing the differential overall survival (OS) between (F) FGFR1-low and FGFR1-high samples or (G) PARP1-low and PARP1-high samples from the TCGA pancreatic adenocarcinoma cohort.