Skip to main content
. 2012 Mar 20;22(6):1003–1021. doi: 10.1038/cr.2012.44

Figure 1.

Figure 1

SRC-3 regulates MIF expression. (A) Immunoblot analysis demonstrated specific knockdown of SRC-3, but not SRC-1 or SRC-2, in MCF-7 cells by infection with lentivirus expressing shRNA against SRC-3. (B) Knockdown of SRC-3 abolished the induction of PRs (PR-A and PR-B) by estradiol. (C) Schematic representation of the strategy used to identify genes that promoted cell survival in MCF-7 breast cancer cells under SRC-3 knockdown condition. (D) Immunoblot analysis showed that compared to transfection with control siRNA, transfection of siRNAs against SRC-3 (siSRC-3) suppressed MIF protein expression. β-actin was used as loading controls. (E) Semi-quantitative RT-PCR showed that the MIF mRNAs were reduced in SRC-3 knockdown cells. GAPDH was used as loading controls. (F) Expression of MIF protein in mammary epithelial cells derived from SRC-3-null mutant (SRC-3–/–) mice was reduced compared to wild-type cells. β-actin was used as loading control. (G) Levels of Mif mRNA from MEFs and primary lymphocytes from wild-type (SRC-3+/+) or null mutant (SRC-3–/–) mice were compared by RNase protection assay (RPA). L32 and GAPDH were used as loading controls. All normalized intensity is quantified by ImageJ.