Recent studies have demonstrated the overexpression and amplification of miR-17-92 cluster in many malignant human cancers,including B-cell lymphomas and lung cancers.The purpose of this study was to investigate the expression of miR-17-92 cluster in esophageal squamous cell carcinoma for the first time.We detected miR-17-92 cluster was overexpressed in 21 of 28(75%) esophageal cancer samples and all 7 esophageal cancer cell lines.miR-17-92 cluster could promote cell growth in vivo and in vitro.By miRNA-specific quantitative real-time reverse transcriptase-polymerase chain reaction(miR-qRT-PCR),the highest expression level of these five miRNAs is miR-92-1, followed by miR-20a,miR-17-5p,miR-19a and miR-18a.However,inhibition of miR-19a by antisense oligonucleotides(ONs) could induce apoptosis.In marked contrast, antisense ONs against miR-17-5p,miR-18a,miR-20a and miR-92-1 did not exhibit such significant inhibitory effects.Through Human Apoptosis RT Profiler PCR Array 384HT (370 genes),we found 19 genes was up-regulated more than 2-fold,when transfected with miR-19a antisense ONs compared with the control scramble ONs.TNF was 12-fold up-regulated.Combined with bioinformatics target prediction,miR-19a has a complementarity to the 3\'UTR of TNF mRNA.We also identified TNF as a novel direct target of miR-19a by reporter assay.Taken together,we conclude that miR-17-92 cluster is overexpressed in esophageal squamous cancer and miR-19a may involve in this tumorigenesis. Previously we showed that End-binding protein 1(EB1) may promote cellular growth by activatingβ-catenin/T-cell factor(TCF) pathway.To further investigate the role of EB1 in regulating cellular growth,we established an EB1-inducible expression system.The protein level of EB1 was significantly up-regulated upon doxycycline induction.We found that EB1 promoted cellular growth and resulted in a significant increase in colony formation.In addition,EB1 could induce tumor formation in nude mice,activateβ-catenin-dependent gene expression and up-regulate the transcriptional activity of c-Myc.We also showed that EB1 in this manner inhibited apoptosis of 293-T-REx cells upon cisplatin and up-regulated expression of Bcl-2,whereas delta N-TCF4,an inhibitor ofβ-catenin/TCF pathway,could completely or partially abolish the effects of EB1 on the promotion of cell growth and the inhibition of apoptosis activity. Moreover,knockdown of c-Myc by RNAi could abrogate up-regulation of EB1-dependent induction of Bcl-2 expression.Overall,EB1 acts as a potential oncogene via activatingβ-catenin/TCF pathway to promote cellular growth and inhibit apoptosis.