Data Availability StatementData sharing is not applicable to this article as no datasets were generated or analysed during the current study. used to measure LATS2 and TAZ expression in normal and ESCC tissue. Results LATS2 is usually a component of the Hippo tumor-suppressive signaling pathway. Frequent loss of heterozygosity of LATS2 has been reported in esophageal cancer. We analyzed the reciprocal expression legislation of miR-31 and LATS2 and confirmed that LATS2 appearance was raised by down-regulation of miR-31 on the post-transcriptional level in ESCC. Furthermore, miR-31 considerably suppressed the luciferase activity of mRNA combined with LATS2 3-UTR, an integral molecule within the Hippo pathway. After that, LATS2 marketed the translocation of TAZ therefore, which was analyzed using immunohistochemistry. Silencing of miR-31 inhibited the cell proliferation, induced apoptosis and reduced the power of migration/invasion in vitro. LATS2 impedes ESCC cell invasion and proliferation by suppressing miR-31, in addition to mice xenograft model in vivo. On the other hand, the nuclear localization of LATS2 constrained the phosphorylation of TAZ. After that, the appearance degree of TAZ was notably heightened with a higher threat of recurrence in comparison to that seen in the low-risk sufferers, in addition to, the higher appearance associated with an unhealthy success. Conclusions Our research confirmed that overexpression of miR-31 undertook an oncogenic function in ESCC by repressing appearance of LATS2 via the Hippo Pathway and activating epithelial-mesenchymal changeover. LATS2 and TAZ could possibly be potential book molecular markers for predicting the chance of prognosis and recurrence of ESCC. Electronic supplementary materials The online edition of this content (10.1186/s13046-017-0622-1) contains supplementary materials, which is open to authorized users. solid course=”kwd-title” Keywords: miR-31, LATS2, Hippo pathway, TAZ, EMT, Esophageal squamous cell carcinoma Background Esophageal cancers is among the most popular sorts of malignant tumor, that is the 6th leading reason behind cancer-related fatalities within the global globe and third in China [1, 2]. Esophageal squamous cell carcinoma (ESCC), the predominant histologic subtype of esophagus cancers, is widespread in Asia, accounting for 90% situations specifically in China [3C5]. Because of a spectral range of aberrantly intense phenotypes and lack of early detection, most of the patients are diagnosed with advanced disease and have to give up the main curative option of surgical resection. Despite recent improvements in multimodality therapies, the prognosis remains dismal. Like other malicious tumors, the pathogenesis and progression of ESCC are a long procedure including activation of oncogenes and/or inactivation of tumor suppressor genes. Recently, promising molecular genetic alterations with clinical end result in ESCC have been predicted [6, 7]. Therefore, specific molecular markers associated with the progression and therapeutic targets are immediately needed for patient classification and the improvement of N-Acetylornithine individualized therapy regimens. MicroRNAs (miRNAs) are a class KRAS of highly-conserved, non-coding RNAs of 18 to 25 nucleotides in length and could function as indispensable and unfavorable regulators of gene expression at the post-transcription level. The mature forms of miRNAs silence the gene expression by binding to the 3-untranslated region (3-UTR) of mRNAs and initiate the N-Acetylornithine translational repression and/or target them for degradation. Mounting evidences show that miRNAs can donate to the malignant tumor progression and metastasis process, such as cell proliferation, invasion, angiogenesis, and the epithelial to mesenchymal transition (EMT) N-Acetylornithine [8C10]. Among the most frequently altered miRNAs recognized, miR-31, which is located on the common homozygous deletion region on chromosome 9p21.3, is emerging as a complex player in an ocean of cancers. Evidence proposes that miR-31 can function as either an oncogene or a tumor suppressor in type-specific cancers, respectively. For example, increased expression of miR-31 has been recognized in colorectal , lung malignancy and HNSCC , whereas it plays a tumor-suppressive role in ovarian  prostate , breast malignancy  and melanoma . Moreover, downregulation of miR-31 in esophageal adenocarcinoma (EAC) correlates with poor prognosis [18, 19]. Inversely, miR-31 is usually up-regulated in tissue and serum samples of ESCC, with expression relating to staging . Still, in another ESCC miR-31 expression was diminished . These studies highlight the complexity of miR-31-associated malignant phenotypes. Challenges have N-Acetylornithine to be resolved before miR-31 could be investigated in clinical trials, including N-Acetylornithine definition of miR-31 targets, as well as pathways regulating miR-31 appearance in ESCC. The Hippo pathway can be an evolutionarily conserved pathway that exerts deep effects in the legislation of body organ size, tumorigenesis, embryonic advancement, stem cell homeostasis, and epithelial to mesenchymal changeover . Among the cores of Hippo signaling complicated in mammals is certainly Lats1 or Lats2 (Lats1/2) kinases, others including MST1/2, YAP1 and MOB1 [23, 24]. LATS2 kinases are associates from the LATS/NDR kinase family members, which encodes a serine/threonine proteins kinase owned by.