Fig 1: Tumor-suppressive effects of human macrophage-derived CM and atypical tumor-suppressing proteins (Hsp90ab1, enolase 1, and ubiquitin C). Macro CM = human macrophage-derived conditioned medium, CM = RAW264.7 osteoclasts-derived conditioned medium, BM = BML284 treated, CN = control, Hab1 = Hsp90ab1, Eno1 = enolase 1, and Ubc = ubiquitin C. * p < 0.05 and ** p < 0.01 (A,B) Reduction in EdU-based proliferation and transwell invasion of MDA-MB-231 breast cancer cells by BM Macro CM. (C) Downregulation of Lrp5, Runx2, and TGFβ in BMD-MB-231 breast cancer cells by BM Macro CM. (D) Shrinkage of human breast cancer tissue fragments by BM Macro CM. (E) Elevation of Hsp90ab1, enolase 1, and ubiquitin C in BM CM. (F) ELISA-based concentrations of Hsp90ab1, enolase 1, and ubiquitin C in BM CM. (G) Selective inhibition of the MTT-based viability of MDA-MB-231 cancer cells by recombinant Hsp90ab1, enolase 1, and ubiquitin C, compared to three lines of human breast epithelial cells (KTB34, KTB22, and KTB6).
Fig 2: Tumor-suppressing proteins in CW008-treated mesenchymal stem cell (MSC) CM.The single and double asterisks indicate p<0.05 and 0.01, respectively. CM = conditioned medium, CW = CW008 (PKA activator), CALR = calreticulin, ENO1=enolase 1, HSP = heat shock protein 90ab1, MSN = moesin, UBC = ubiquitin C, MMP2 and MMP9=matrix metalloproteinases 2 and 9, Col I=type I collagen. (A) Western blot-based expression levels of CALR, ENO1, HSP, MSN, UBC, MMP2, MMP9, and Col I in CW008-treated MSC CM. (B–F) ELISA-based levels of five tumor-suppressing proteins (CALR, ENO1, HSP, MSN, and UBC) in CW008-treated MSC CM (n=3). (G) Dose responses of TT2 OS cells in response to CW008-treated MSC CM with IC50 at 390 μg/ml (n=5). (H) Dose responses and IC50 of TT2 OS cells in response to five tumor-suppressing proteins (CALR, ENO1, HSP, MSN, and UBC). (Error bars indicate standard deviation.) Figure 4—source data 1.Original files for the gels in Figure 4A.
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