Skip to main content
. 2022 Dec 25;15(1):124. doi: 10.3390/cancers15010124

Figure 4.

Figure 4

Autocrine activation of the CXL10/CXCR3 pathway by endogenous CXCL10 in EGFR-mutant lung cancer cells. (A) Supernatants collected from HCC4006 and HCC827 cells treated with 20 pg/mL IFN-γ for 72 h were analyzed using ELISA for CXCL10 (* p < 0.5 and ** p < 0.01 versus control). (B) Increased CXCL10 mRNA expression of HCC 4006 with coculture and treatment of EGFR-TKI. (C–E) HCC4006 and HCC 827 cells cocultured with activated PBMCs for 48 h and treated for 6 h with siRNA against endogenous CXCL10. (C) ELISA quantification for CXCL10 of supernatants from coculture with activated PBMC (* p < 0.05). (D) Western blot analysis of samples treated with siRNA against CXCL10. € Immunofluorescence analysis of p-p65 and HIF-1α in cells treated with siRNA CXCL10 or erlotinib (50 nM, HCC4006 cell and 20 nM HCC827 cells). Nuclei were counterstained with DAPI (blue) for the detection of DNA. Data are presented as mean ± SD of three independent experiments. Cells were treated with 100 µM of each of the STAT3 and HIF-1α inhibitors.