Mammalian enabled homolog (ENAH) (Mena)

The Mammalian enabled homolog (Mena, also known as ENAH) is an actin regulatory protein belonging to the Ena/VASP family, encoded by the ENAH gene on chromosome 1, that controls actin filament nucleation, polymerization, and dynamics to regulate cytoplasmic actin networks.[1][2][3][5] It localizes to lamellipodia, filopodia tips, cell-cell contacts, and focal adhesions, influencing cell motility, adhesion, migration, and invasion through antagonism of actin capping proteins and stabilization of invadopodia.[1][2][3][5] Mena undergoes alternative splicing to produce isoforms like pan-Mena, Mena^11a (epithelial-like, invasion-suppressive), and invasive variants (Mena^INV, Mena^++, Mena^+++ , hMENAΔv6) that switch during tumor progression, with invasive forms upregulated in mesenchymal phenotypes and metastases.[1][2][3] Overexpression of Mena and specific isoforms correlates with premalignant lesions, tumor grade, lymphatic metastasis, poor prognosis, and EMT markers (e.g., reduced E-cadherin, increased vimentin, MMP-2) in cancers including breast, colorectal, gastric, cervical, salivary gland, oral squamous cell carcinoma, and hepatocellular carcinoma.[1][3][7][8][9] While Mena promotes proliferation, invasion, and metastasis, its deficiency reduces tumor cell motility and delays metastatic dissemination without affecting primary tumor growth, suggesting potential as a prognostic biomarker rather than a direct therapeutic target.[1][2][11] Interactions with pathways like EGF/HER2, PDGF/PI3K, and Wnt/β-catenin further link it to oncogenic signaling and microenvironment-driven invasion.[1][2]

Other names

ENAHProtein enabled homologhMenapan-MenaMena^11aMena^INVMena^++Mena^+++hMENAΔv6