Fig. 3: Nalcn deletion does not impact the incidence, tumor-free survival or growth rates of P1KP, V1KP or Pdx1KP primary tumors.
From: The NALCN channel regulates metastasis and nonmalignant cell dissemination
a–c Tumors and representative photomicrographs (H&E from all tumors (left; Supplementary Table 9) and dual immunofluorescence from five independent tumors each (right)) for lineage tracing (ZSG), epithelial (CK7, CK20) and EMT markers (CDH2, CDH1) of P1KP-GAC (a), V1KP-IAC (b) and Pdx1KP-PAC (c). Scale bar, 50 μm. Single-channel images are shown in Supplementary Fig. 1. d–g, Upper: organ heatmaps of tumor incidence in P1KP at P3 and V1KP at mice of each Nalcn genotype recombined at P3 (d,e) or P60 (f,g). Lower: survival curves of mice in each cohort. Male to female ration (M:F) is shown. P1KP P3, P = 0.6912; P1KP P60, P = 0.3897; V1KP P3, P = 0.1900; and V1KP P60, P = 0.8301. Mantel–Cox test. h, Organ primary tumor heatmaps and survival curves of Pdx1KP mice (P = 0.1095). Mantel–Cox test. Source data for d–h are given in Supplementary Table 9. i, Growth rates of P1KP-GAC (n = 38), V1KP-IAC (n = 57) and Pdx1KP-PAC (n = 28) tumors. Two-tailed Mann–Whitney U-tests revealed no significant difference in growth rates among tumors with different Nalcn genotypes P1KP-GAC: Nalcn+/+ (n = 11) versus Nalcn+/Flx (n = 18; P = 0.912), versus NalcnFlx/Flx (n = 9; P = 0.7103). V1KP-IAC: Nalcn+/+ (n = 16) versus Nalcn+/Flx (n = 25; P = 0.5169), versus NalcnFlx/Flx (n = 16; P = 0.7309). Pdx1KP-PAC: Nalcn+/+ (n = 10) versus Nalcn+/Flx (n = 13; P = 0.7844), versus NalcnFlx/Flx (n = 5; P = 0.1292). Bar, median. Source data are given in Supplementary Table 10. j, Gene set enrichment analyses of transcriptomes of Nalcn+/Flx and NalcnFlx/Flx P1KP-GAC, V1KP-IAC and Pdx1KP-PAC versus Nalcn+/+ tumors.
