Extended Data Figure 8: Gap-junction-generated signalling activates IFN and NF-κB pathways in cancer cells.
From: Carcinoma–astrocyte gap junctions promote brain metastasis by cGAMP transfer
a, Cytokine array analysis of conditioned media collected after 24 h co-culture of human astrocytes with control or Cx43-depleted MDA231-BrM2 cells. The log2 fold changes are plotted. b, Schematic of co-culture conditioned media collection and human astrocyte re-isolation (left) ELISA of IFNα and TNF in conditioned media from astrocyte co-cultures with the indicated MDA231-BrM2 cells (right) Data are mean ± s.e.m. (n ≥ 2 independent experiments with 4 total replicates). c, Relative levels of cleaved caspase 3 in MDA231-BrM2 cells treated with various concentrations of carboplatin in the presence or absence of 10 U ml−1 (39 U ng−1) IFNα or 10 pg ml−1 TNF. Data are mean ± s.e.m. (n = 5 technical replicates over 3 independent experiments). d, STAT1 levels in control and STAT1-knockdown LLC-BrM and 393N1 cells. e, Quantification of BLI signal from brain metastases formed by syngeneic LLC-BrM control, or STAT1-knockdown cells (n = 2 independent experiments with 12–15 mice total per group). f, NF-κB Renilla luciferase reporter assay in MDA231-BrM cells expressing control pBABE or SR-IκBα vector. Data are mean ± s.e.m. (n = 3 technical replicates).
