Conclusions
Our findings suggest that silencing ADRM1 induces osteoblast mineralization and differentiation by activating the Wnt/β-catenin pathway. This finding underscores the therapeutic potential of the ADRM1/Wnt/β-catenin axis in treating OP.
Methods
In vitro experiments, including both gain-of-function and loss-of-function approaches, were conducted in MC3T3-E1 and C3H10T1/2 cells.
Objective
Adhesion regulating molecule-1 (ADRM1), a 26S proteasome adaptor protein, plays a crucial role in mediating the growth and differentiation of osteoclasts in osteoporosis (OP). However, its involvement in this osteoanabolic effect remains largely uninvestigated.
Results
Knockdown of ADRM1 markedly promoted the growth of C3H10T1/2 cells while inhibiting apoptosis. Additionally, this intervention enhanced the expression of osteoblast differentiation markers and key proteins associated with the Wnt/β-catenin pathway. Notably, silencing ADRM1 promoted osteoblast mineralization and differentiation, as evidenced by increased Alizarin red staining and alkaline phosphatase staining. Conversely, MC3T3-E1 cells overexpressing ADRM1 exhibited results that were diametrically opposed to those observed with ADRM1 knockdown. Furthermore, treatment with ICG-001 (a Wnt/β-catenin pathway antagonist) reversed the effects of ADRM1 knockdown in C3H10T1/2 cells. Conclusions: Our findings suggest that silencing ADRM1 induces osteoblast mineralization and differentiation by activating the Wnt/β-catenin pathway. This finding underscores the therapeutic potential of the ADRM1/Wnt/β-catenin axis in treating OP.