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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Cancer Res. 2016 Oct 1;76(19):5657–5670. doi: 10.1158/0008-5472.CAN-15-2616

Figure 7.

Figure 7

Inhibition of GRP78 and GRP78-regulated cellular metabolites affect innate immunity. A. Serum from LCC9 xenograft-bearing female aythmic mice untreated (control) and treated TAM, LA, LA+TAM and serum from untreated or GRP78 morpholino treated female BALB/c mice were analyzed by ELISA for circulating systemic levels of MCP-1. n=4, *p<0.001. B. Protein lysates from LCC9 tumors (control, TAM, LA, or LA+TAM) were analyzed using Western blot hybridization for calreticulin, HMGB1, and self-recognition identifier CD47. C. Protein lysates from LCC9 tumors (control, TAM, human targeting GRP78M, or human targeting GRP78M+TAM) were analyzed using Western blot hybridization for calreticulin, HMGB1, and self-recognition identifier CD47. E. Protein lysates from mammary glands extracted from untreated or GRP78M treated female BALB/c mice were analyzed for calreticulin and CD47. Gel loading was confirmed by measuring actin expression. Treated LCC9 tumor sections (D) or mammary glands from untreated or GRP78 morpholino (GRP78M) treated BALB/c mice (F) were stained using CD68 antibody to determine macrophage infiltration and visualized at 40x.