Fig. 7.

Overexpression of β-catenin reverses the effect of MICALL2 knockdown on CRC. A Western blotting was used to examine the expression of MICALL2 and β-catenin in the MICALL2-silenced HCT8 and control cell line transfected with β-catenin-expressing plasmids. GAPDH was used as an internal control. B Growth curves of MICALL2-silenced HCT8 and control cell line transfected with β-catenin-expressing plasmids. C Representative images (left) and quantification of wound area (right) of gap closure of MICALL2-silenced HCT8 and control cell line transfected with β-catenin-expressing plasmids, respectively. D A working model for MICALL2 functions in colorectal cancer cells. In the normal colonic epithelial cells, TRIM21 binds to MICALL2 and promotes the ubiquitination and degradation of MICALL2, thereby suppressing the growth and migration of normal colonic epithelial cells. However, in colorectal cancer cells, reduced TRIM21 expression leads to decreased ubiquitination and degradation of MICALL2, as a result, the up-regulated MICALL2 promotes the tumorigenesis of colorectal cancer via the Wnt/β-catenin signaling pathway