ABSTRACT Suppressor of cytokine signaling 2 (SOCS2) is a classical feedback inhibitor of JAK–STAT signaling, but its role in porcine adipose‐derived mesenchymal stem cells (PADSCs) and fat deposition remains unclear. Here, we investigated the function and mechanism of SOCS2 in PADSC proliferation and adipogenic differentiation. SOCS2 overexpression reduced colony number, slowed CCK‐8 growth curves, and induced G0/G1 arrest, whereas SOCS2 knockdown enhanced proliferation and promoted the G1/S transition. In parallel, SOCS2 overexpression decreased lipid droplet accumulation and downregulated adipogenic markers, while SOCS2 silencing produced the opposite effects, indicating that SOCS2 negatively regulates both PADSC expansion and adipocyte formation. Transcriptomic analysis showed that SOCS2 mainly influenced pathways related to extracellular matrix organization, cell cycle, and cytokine/inflammatory signaling. At the protein level, SOCS2 silencing increased total JAK2 and STAT3, whereas SOCS2 overexpression reduced JAK2 abundance and STAT3 activation, accompanied by concordant changes in Cyclin D1, CDK2, and PCNA. Collectively, these results suggest that SOCS2 exerts dual negative effects on PADSC proliferation and adipogenic differentiation, accompanied by changes in JAK2‐STAT3 signaling. These findings provide functional evidence supporting SOCS2 as a candidate gene related to porcine fat deposition and provide a basis for further genetic validation in pig breeding populations.
Shi et al. (Mon,) studied this question.