Supplementary Figure S3 from A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling

Figure S3: Extended data for Fig 3 - SM expression can be regulated by a STING-IFNβ signaling axis. (A-C) Tables summarizing statistical comparisons for densitometry analysis of western blots from (A) Log2FC in expression levels compared to 4T1P controls in Fig 3A, (B) Log2FC in expression levels compared to vehicle-treated control in Fig 3D, and (C) Log2FC in expression levels in EMT6M and EMT6CaR vs. vehicle controls in Fig 3J (n=3 for all; Supplemental Data File 3 shows blotting replicates) (D) Protein expression analysis of the STING pathway in EMT6M tumor cells following treatment with Ax, Ca, or DMXAA evaluated by western blot (n=2-3). (E) Table summarizing statistical comparisons for densitometry analysis of western blot from Fig S3D. (F-G) Ifnb gene expression evaluated by qRT-PCR in: (F) 4T1AxR vs. 4T1P (n=3). (G) EMT6CaR vs. EMT6M (n=3). (H) Log2FC comparison of SM expression in EMT6shCon or EMT6IFNAR1-KD cells before and after Ax or Ca treatment as shown in Fig 3O (n=3). Metastatic parental control for EMT6CaR (EMT6M); Parental (P); shRNA Vector control (shCon); Axitinib-resistant (AxR); Cabozantinib-resistant (CaR); Interferon-beta (Ifnβ); Type I IFN receptor knockdown (IFNAR1-KD); Standard deviation (SD); Drug concentrations for SN-011 (6µM), MSA-2 (33µM), DMXAA (50µM), Ax (0.5µM), Ca (2µM), Su (2µM), Tivo (2µM), Pazo (2µM), and Lenv (2µM). Quantitative data is shown as mean ± SD; * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.