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. 2018 Feb 13;12(3):391–405. doi: 10.1002/1878-0261.12173

Figure 6.

Figure 6

MAD2L2 knockdown promoted CRC growth in a mouse xenograft model and MAD2L2‐regulated NCOA3 phosphorylation, ubiquitination, and degradation in CRC cells. Nude mice were subcutaneously injected with HCT116 cells with nonspecific siRNA (NC), MAD2L2 knocked down by its specific shRNA (sh1), vector, MAD2L2 overexpression (MAD2L2), MAD2L2 +  vector, MAD2L2 +  NCOA3 overexpression (NCOA3). (A) Images of the CRC tumor xenograft from each mouse (n = 5 mice/group). (B) Tumor weights were analyzed. *P < 0.05 (n = 5) (C, D) Tumor volumes were recorded and analyzed. ***P < 0.001 (n = 5) (E) The expression of MAD2L2 and NCOA3 in tumor tissues was analyzed by IHC staining. (F) (1) MAD2L2 had elevated expression in response to the increased DNA damage and chromosome instability in CRC cells. (2) MAD2L2 activated p38. (3) p‐p38 phosphorylated NCOA3. (4) Phosphorylated NCOA3 was ubiquitinated. (5) Ubiquitinated NCOA3 was degraded by the proteasome.