Fig. 8

RGS12 promotes the degradation of KIF2A through MYCBP2. a, b TAMs were extracted from the RGS12 cKO mice or WT mice with oral cancer. The TAMs of WT mice were stably transfected with pCMV or pCMV-RGS12 plasmids. The cell lysates of TAMs were incubated with anti-MYCBP2 or IgG antibodies, and bound protein was detected by immunoblotting with the KIF2A antibody. **P < 0.01, ***P < 0.001, n = 3. c TAMs from oral cancer tissues of WT mice were stably transfected with pCMV (Ctrl) or pCMV-RGS12 (RGS12 OE) plasmids. Then, the TAMs were treated with PKC412 (1 μmol·L⁻¹, tyrosine kinase inhibitor, Cayman) for 24 h. The cell lysates were incubated with anti-p-Tyr or IgG antibodies, and bound protein was examined by immunoblotting with the MYCBP2 antibody. Cell lysates were also immunoblotted with anti-KIF2A and anti-β-Actin. **P < 0.01, ***P < 0.001, n = 3. d TAMs from oral cancer tissues of WT mice were treated with pCMV (Ctrl) or pCMV-RGS12 (RGS12 OE) or pCMV-RGS12 + shMYCBP2 (RGS12 OE + shMYCBP2). Cell lysates were immunoblotted with anti-KIF2A, anti-Ub, and anti-β-Actin. Data are expressed as mean ± SEM (n = 3, *P < 0.05, ***P < 0.001)