N-cadherin plays a critical role in cancer progression by promoting epithelial-to-mesenchymal transition (EMT), which enhances tumor cell migration and metastasis. Its expression is associated with increased invasiveness in solid tumors and contributes to hematological malignancies by aiding bone marrow homing and protecting cancer cells from chemotherapy. N-cadherin interacts with key signaling pathways, including FGFR and Wnt/β-catenin, supporting cancer cell survival and proliferation. Due to its involvement in metastasis and therapy resistance, it is being explored as a potential target for cancer treatment. [1]
The ABclonal A19083 [KO Validated] N-Cadherin Rabbit mAb was cited in a study by Dr. Yin and Dr. Zhang from Northwestern Polytechnical University, titled Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway, published in Research (Wash D C) on Feb 28, 2024. The study found that CCDC150 knockdown in triple-negative breast cancer (TNBC) cells significantly reduced N-cadherin expression while increasing E-cadherin, inhibiting EMT and metastatic potential. This suggests that targeting CCDC150 can suppress metastasis by downregulating N-cadherin, reducing TNBC cell invasion and migration.
