Fig. 8: Ectopic SBDS suppresses tumor growth in vivo.
From: Dual regulation of p53 by the ribosome maturation factor SBDS
a Ectopic SBDS does not affect body weights of the mice bearing tumors derived from HCT116p53+/+ cells. b Ectopic SBDS suppresses growth of the xenograft tumors derived from HCT116p53+/+ cells in vivo. c Representation of the dissected tumors derived from HCT116p53+/+ cells expressing the empty vector or ectopic SBDS. d, e Ectopic SBDS activates p53 pathway in tumors derived from HCT116p53+/+ cells. The tumors were homogenized and lysed for qRT-PCR d or IB analysis e. f Ectopic SBDS does not affect body weights of the mice bearing tumors derived from HCT116p53−/− cells. g Ectopic SBDS does not affect growth of the xenograft tumors derived from HCT116p53−/− cells in vivo. h Representation of the dissected tumors derived from HCT116p53−/− cells expressing the empty vector or ectopic SBDS. i, j Ectopic SBDS does not affect p53 target gene expression in tumors derived from HCT116p53−/− cells. The tumors were homogenized and lysed for qRT-PCR i or IB analysis j. k Working model of dual regulation of p53 activity by SBDS. Under the normal culture condition, SBDS mostly reside in the nucleolus and cytoplasm to conduct oncogenic function by boosting ribosome biogenesis and maintaining p53 at a low expression level (upper panel). In response to ribosomal stress, SBDS translocates to the nucleoplasm to execute a tumor-suppressive role by interacting with p53 and dissociating the MDM2–p53 complex (lower panel).
