MME (membrane metalloendopeptidase), also known as CD10 or neutral endopeptidase (NEP), is a cell surface zinc-dependent enzyme encoded by the MME gene. It plays a critical role in regulating bioactive peptides by degrading substrates such as atrial natriuretic peptide (ANP), enkephalins, and bradykinin, thereby modulating blood pressure, pain perception, and immune responses. MME is expressed in various normal tissues, including epithelial cells, fibroblasts, and lymphoid progenitors, and is particularly prominent in organs like the kidney, lung, and intestine.
In pathological contexts, MME has dual roles in cancer. It acts as a tumor suppressor in certain malignancies (e.g., prostate cancer) by inhibiting signaling pathways linked to proliferation and angiogenesis. Conversely, its overexpression in cancers like acute lymphoblastic leukemia (ALL), follicular lymphoma, and some solid tumors (e.g., breast carcinoma) is associated with aggressive phenotypes and poor prognosis. MME/CD10 is a well-established diagnostic marker for ALL and germinal center-derived lymphomas.
Therapeutically, MME is explored as a target for prodrug activation and antibody-based therapies. Research also focuses on its role in tumor microenvironments and immune regulation. As a research tool, MME-specific antibodies are vital for immunohistochemistry, flow cytometry, and functional studies to dissect its biological and clinical significance. Its dynamic expression across tissues and diseases underscores its importance in both physiology and pathology.