NELL-1 was a secreted protein,originally detected to be upregulated in pathologically fusing and fused sutures in non-syndromic unilateral coronal synostosis (UCS) patients.△part from its special ability of osteogenesis in long and craniofacial bone,it had been researched to inhibit formation of benign and malignant tumors including Burkitts lymphoma,colorectal adenocarcinoma,esophageal adenocarcinoma,et al.In our previous study,we identified a new transcripts of NELL-1.As lacing a calcium-binding EGF-like domain compared with the NELL-1 full length,we named the new transcript NELL-1-△E.These two transcripts had similar expression pattern both in intra and extra cell in protein level and similar intracellular localization.However,Nell-1-△E had different space-time expression than Nell-1 full length in mice embryos skull.Via homology modeling,we found that there were three obvious structural differences between the two transcripts.Furthermore,when treating cancer cells by NELL-1 full length or NELL-1-△E protein,we observed only NELL-1-△E exhibited the capacity to depress the migration of cells.Similar result was found when overexpressing the two transcripts in vitro.We found that NELL-1-△E interacted with enolase-1 (ENO-1) in extra cells in two cell lines by co-immunoprecipitation and LC-MS/MS.ENO-1 was shown to be overexpressed in many human cancers and played an important role in tumorigenesis.NELL-1-△E might serve as a substrate of ENO-1 by interacting with it,therefore inhibits migration of cells as a suppressor gene.