Furthermore, in breast cancer–associated fibroblasts (CAFs), SNHG5 stabilizes ZNF281 mRNA through an m6A-dependent mechanism, upregulating CCL2/CCL5 expression and activating p38 MAPK signaling, which enhances vascular permeability and neovascularization to facilitate PMN formation [62]. Here, CCL2 is linked to breast carcinoma.