Moreover, IMR-1 induced E-cadherin and inhibited N-cadherin, Vimentin, and Snail, curbing EMT process, suggesting that inhibition of the Notch signaling pathway could partially counteract functions of lncRNA NEAT1 and VEGF-A, consequently inhibiting cell proliferation and EMT process while enhancing apoptosis in OSCC, which is in consistence with the previous finding that IMR-1 could inhibit the growth of patient-derived tumor xenografts [24]. Here, CDH2 is linked to neoplasm.