Figure 6.

USP9X-mediated stabilization of TTK promotes tumorigenesis in NSCLC. TTK is targeted for proteasome-dependent degradation by E3 ubiquitin ligase APC-c. USP9X decreases ubiquitination of TTK, and thereby enhances its half-life. Overexpression of USP9X would increase TTK levels and subsequently promote cell proliferation, migration and invasion. Immunohistochemistry experiments on clinical samples of NSCLC showed that elevated USP9X in NSCLC patients dramatically increases TTK levels and thus promotes tumor growth.