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. Author manuscript; available in PMC: 2013 Oct 25.
Published in final edited form as: Oncogene. 2012 Jun 18;32(17):2169–2178. doi: 10.1038/onc.2012.238

Figure 1. Ectopic expression of RNPC1 inhibits MDM2 expression independent of p53.

Figure 1

(A–B) The level of MDM2 protein is decreased by RNPC1 in HCT116 (A) and RKO (B) cells. HCT116 (A) and RKO (B) cells were uninduced or induced with 0.25 μg/ml tetracycline to express RNPC1 for 24 h. Cell lysates were collected and the level of RNPC1, MDM2, and actin was analyzed by Western blot analysis. The level of MDM2 protein was normalized to that of actin control and the fold change was shown below each lane. Data are representative from three independent experiments. (C) Ectopic expression of RNPC1b does not affect MDM2 expression. The level of RNPC1b, MDM2, and actin was determined in RKO cells uninduced or induced to express RNPC1b for 24 h. The level of MDM2 protein was normalized to that of actin control and the fold change was shown below each lane. (D–E) Over-expression of RNPC1 inhibits MDM2 expression in p53-null cells. p53−/− HCT116 (D) and H1299 (E) cells was uninduced or induced to express RNPC1 for 24 h, followed by Western blot analysis to determine the level of RNPC1, MDM2, MDMX, and actin. The level of MDM2 and MDMX protein was normalized to that of actin control, respectively, and the fold change was shown below each lane. Data are representative from three independent experiments. (F) The experiment was performed as in (E) except that SW480 cells were uninduced or induced to express RNPC1 for 24 h. The relative fold change was shown below each lane. Data are representative from three independent experiments.