In comparison, GCT-Bs showed higher expression of p63 (14 of 15 cases with >50% of positive mononuclear cells), RANKL, and SATB2, whereas CD14, CD33, RANK and RUNX2 were similarly expressed.
In the functional aspect, overexpression of FLNBv4 led to upregulation of RANKL, OCN, OPG and RUNX2, which are closely related to GCT cell survival and differentiation.
However, upregulation of miR-30a expression reduced the RunX2 protein expression level, and downregulation of miR-30a expression reversed the anticancer effect of imatinib on GCT, increasing the expression level of RunX2 protein in GCT.