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. Author manuscript; available in PMC: 2024 May 1.
Published in final edited form as: Clin Cancer Res. 2023 Nov 1;29(21):4464–4478. doi: 10.1158/1078-0432.CCR-23-1439

Fig. 2. Upregulation of non-canonical STING-NF-κB/STAT3, canonical cGAS-STING and activation STAT3-HMG secretory pathways in SPOP mutant (SPOPF102C/SPOPF133V)-expressing prostate cancer cells.

Fig. 2.

A. Targeted proteomics analysis of Dox-inducible SPOPwt and SPOPmut C4–2b and RM-1-BM prostate cancer models yielded 81 protein features that were differentially expressed between SPOPmut (F102C and F133V) C4–2b prostate cancer cells compared to SPOPwt or empty vector controls (upper panel). Ingenuity Pathway Analyses of these 81 proteins revealed enriched representation of NF-κB-centric protein network features (lower panel). B, C. Immunoblot analysis of proteins involved in non-canonical STING-NF-κB signaling, cGAS-STING signaling and STAT3-HMG secretory regulation pathways in stably transduced SPOPwt- and SPOPmut-(F102C, F133V) expressing or empty vector control C4–2b and RM-1-BM prostate cancer cells.