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Lymph node metastasis (LNM) is a significant barrier to the prognosis of patients with gastric cancer (GC). Helicobacter pylori (H. pylori)-positive GC patients experience a higher rate of LNM than H. pylori-negative GC patients. However, the underlying mechanism remains unclear. Based on the findings of this study, H. pylori-positive GC patients have greater lymphangiogenesis and lymph node immunosuppression than H. pylori-negative GC patients. In addition, miR-1246 is overexpressed in the plasma small extracellular vesicles (sEVs) of H. pylori-positive GC patients, indicating a poor prognosis. Functionally, sEVs derived from GC cells infected with H. pylori deliver miR-1246 to lymphatic endothelial cells (LECs) and promote lymphangiogenesis and lymphatic remodeling. Mechanistically, miR-1246 suppresses GSK3β expression and promotes β-Catenin and downstream MMP7 expression in LECs. miR-1246 also stabilizes programmed death ligand-1 (PD-L1) by suppressing GSK3β and induces the apoptosis of CD8 + T cells. Overall, miR-1246 in plasma sEVs may be a novel biomarker and therapeutic target in GC-LNM., (© 2023 Wiley‐VCH GmbH.)

Neural invasion (NI) is a vital pathological characteristic of gastric cancer (GC), which correlates with tumor recurrence and a worse prognosis. Long noncoding RNAs (lncRNAs) play critical roles in various biological processes. However, the involvement of lncRNAs in NI of GC (GC-NI) remains unclear. DIAPH2-AS1 was upregulated in NI-positive GC tissues, which was confirmed by qRT-PCR. The higher expression of DIAPH2-AS1 predicted NI and worse survival for GC patients. Both in vitro and in vivo experiments, including wound-healing assay, Transwell assay, DRG-GC cells co-culture model, the mouse sciatic nerve model, and the lung metastasis model, indicated that DIAPH2-AS1 promoted the migration, invasion, and NI potential of GC cells. Mechanistically, pulldown assay and RNA immunoprecipitation assay revealed that DIAPH2-AS1 interacted with NSUN2. Subsequent experiments indicated that DIAPH2-AS1 stabilized NSUN2 from ubiquitin-proteasomal degradation via masking the K577 and K579 of NSUN2. The protection of DIAPH2-AS1 on NSUN2 improved the stability of NTN1 mRNA via m5C modification, which finally induced GC-NI. Our work uncovered DIAPH2-AS1 as a novel oncogenic lncRNA in GC-NI and validated the DIAPH2-AS1-NSUN2-NTN1 axis as a potential therapeutic target for NI-positive GC., (© 2023. The Author(s).)

The purpose of this study was to investigate the effect of miR-702-5p on diabetic encephalopathy (DE) and the interaction of miR-702-5p/12/15-LOX in the central nervous system (CNS). In this study, db/db mice were used as DE animal model and HT22 cells were treated with high-glucose (HG). Based on the bioinformatics prediction of possible binding sites between miR-702-5p and 12/15-LOX, we found that the expression of miR-702-5p was significantly down-regulated while 12/15-LOX up-regulated in vivo and in vitro, and the expression changes were inversely correlated. In vivo, diabetic mice with cognitive dysfunction and hippocampal neuronal damage had a concomitant increase in amyloid precursor protein (APP), amyloid beta(Aβ), tau, BAX protein expressions; by contrast, Bcl-2 protein expression was significantly decreased. Overexpression of miR-702-5p significantly reduced the histopathological damage of the hippocampus, improved the learning and memory function of db/db mice, down-regulated 12/15-LOX, APP, Aβ, tau, BAX protein expressions significantly and up-regulated the expression of Bcl-2. In vitro, miR-702-5p mimic reversed the decline in cell viability and the increase in cell apoptosis induced by HG. Simultaneously, reduced 12/15-LOX, APP, Aβ, BAX protein expressions, and increased Bcl-2 protein expression were detected in the miR-702-5p mimic group. Moreover, combined administration of miR-702-5p mimic and 12/15-LOX overexpression lentivirus significantly reversed the protective effect of up-regulation of miR-702-5p. In conclusion, miR-702-5p has a neuroprotective effect on DE, and this effect was achieved by inhibiting 12/15-LOX. However, miR-702-5p had an endogenous regulatory effect on 12/15-LOX rather than a direct targeting relationship., Competing Interests: Declaration of Competing Interest The authors declare no competing financial interests., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Liver metastasis (LM) is a major obstacle to the prognosis of gastric cancer (GC) patients, but the molecular mechanism underlying gastric cancer liver metastasis (GC-LM) remains unknown. Exosomes have been identified as an important mediator of communication between tumor cells and the microenvironment. Therefore, we sought to investigate the effects of primary GC cells on the liver microenvironment and the role of exosomal microRNAs (exo-miRNA) in GC-LM., Methods: Sequential differential centrifugation, transmission electron microscopy and NanoSight analysis were used to extract and characterize exosomes. MicroRNA sequencing in GC-derived exosomes and mRNA sequencing in PMA-treated THP-1 cells were used to identify differentially expressed miRNAs in exosomes and the functional targets of exosomal miR-519a-3p (exo-miR-519a-3p) in macrophages, respectively. Tracing and internalization of exosomes and transfer of exo-miR-519a-3p were observed by immunofluorescence. Tubule formation assays, aortic ring assays, and exosome-educated GC-LM model were used to investigate the roles of GC-derived exosomes and exo-miR-519a-3p in angiogenesis and GC-LM. Luciferase reporter assay, qRT-PCR, Western blot, ELISA, flow cytometry and immunofluorescence were used to investigate the regulatory mechanism of exo-miR-519a-3p at GC-LM., Results: The expression level of miR-519a-3p in serum exosomes was significantly higher in GC-LM patients than in patients without LM, and high expression of exo-miR-519a-3p indicates a worse prognosis. GC-derived exosomes are mainly accumulated in the liver and internalized by intrahepatic macrophages. Mechanistically, exo-miR-519a-3p activates the MAPK/ERK pathway by targeting DUSP2, thereby causing M2-like polarization of macrophages. M2-like polarized macrophages accelerate GC-LM by inducing angiogenesis and promoting intrahepatic premetastatic niche formation., Conclusions: Our results indicate that exo-miR-519a-3p plays a critical role in mediating crosstalk between primary GC cells and intrahepatic macrophages and is a potential therapeutic target for GC-LM., (© 2022. The Author(s).)

The long noncoding RNAs (lncRNAs) have been investigated in colorectal cancer (CRC). The aim of this study is to identify the biological functions of LBX2-AS1 in CRC. Quantitative real-time polymerase chain reaction was used to examine the expression of LBX2-AS1 in CRC cells. Cell counting kit-8 and colony formation assays were performed to examine cell proliferation. Wound healing and transwell invasion assays were performed to examine the cell migration and invasion. The interaction between PTBP1 and LBX2-AS1 or KAT2A was confirmed by RNA immunoprecipitation. The KAT2A messenger RNA (mRNA) stability was probed using the transcriptional inhibitor Actinomycin D. LBX2-AS1 was significantly increased in CRC tissues and cells. Knockdown of LBX2-AS1 inhibited CRC cell proliferation, migration, and invasion. The notch signaling pathway was activated by LBX2-AS1. LBX2-AS1 enhanced the mRNA stability of the histone acetyltransferase KAT2A by interacting with RNA-binding protein PTBP1. LBX2-AS1 acted as an oncogene in CRC., (© 2022 Wiley Periodicals LLC.)

Circular RNAs (circRNAs) play vital regulatory roles in the progression of multiple cancers. In our study, transcriptome analysis and self-organizing maps (SOM) were applied to screen backbone circRNAs in gastric cancer (GC). Upon validation of the expression patterns of screened circRNAs, gain- and loss-of-function assays were performed in vitro and in vivo. Underlying mechanisms were investigated using RNA pull-down, luciferase reporter assay and RNA immunoprecipitation. The expression of circTHBS1 was significantly increased in GC and associated with poor prognosis. CircTHBS1 facilitated the malignant behavior and epithelial-to-mesenchymal transition of GC cells. Mechanistically, circTHBS1 sponged miR-204-5p to promote the expression of Inhibin Subunit Beta A (INHBA). Moreover, circTHBS1 could enhance the HuR-mediated mRNA stability of INHBA, which subsequently activated the TGF-β pathway. Our research identified circTHBS1 as an oncogenic circRNA that enhances GC malignancy by elevating INHBA expression, providing new insight and a feasible target for the diagnosis and treatment of GC., (© 2022. The Author(s).)

Abnormal cell proliferation caused by abnormal transcription regulation mechanism seems to be one of the reasons for the progression of breast cancer and also the pathological basis. MicroRNA-142-5p (miR-142-5p) is a low-expressed miRNA in breast cancer. The role of MKL-1s regulation of DNMT1 in breast cancer cell proliferation and migration is still unclear. MKL-1 (myocardin related transcription factor A) can bind to the conserved cis -regulatory element CC (A/T) 6GG (called CarG box) in the promoter to regulate the transcription of miR-142-5p. The expressions of miR-142-5p and MKL-1 are positively correlated. In addition, it has been proved that DNMT1 is the target of miR-142-5p, which inhibits the expression of DNMT1 by targeting the 3-UTR of DNMT1, thereby forming a feedback loop and inhibiting the migration and proliferation of breast cancer. Our data provide important and novel insights into the MKL-1/miR-142-5p/DNMT1/maspin signaling pathway and may become a new idea for breast cancer diagnosis, treatment, and prognosis.

Based on the previous studies, this study was carried out to explore the interaction of LncRNA-Malat1/miR-211-5p in cerebral ischemia reperfusion injury (CIRI). Firstly, the expression changes of LncRNA-MALAT1 and miR-211-5p in ischemia patients' blood were determined, and the binding sites of them were predicted by bioinformatics. Furthermore, middle cerebral artery occlusion/reperfusion (MCAO/R) injury model was established in adult male SD rats, and primary neuronal oxygen-glucose deprivation/reoxygen-glucose reoxygenation (OGD/R) was established in vitro. The results showed that LncRNA-MALAT1 was significantly up-regulated and miR-211-5p down-regulated in the peripheral blood of patients with ischemic stroke, and the expression changes were negatively correlated. Bioinformatics prediction results showed that LncRNA-MALAT1 had a binding site with miR-211-5p. We also found that LncRNA-Malat1 was significantly up-regulated while miR-211-5p down-regulated in rat cortex tissue and primary neurons treated with OGD/R. In addition, lentivirus interfered with LV-Malat1-RNAi decreased the expression of LncRNA-Malat1 and promoted the up-regulation of miR-211-5p. Combination of LV-Malat1-RNAi and miR-211-5p inhibitor significantly reversed the protective effect of down-regulation of LncRNA-Malat1. Inhibition of LncRNA-Malat1 expression alleviated the neurological deficit score after MCAO/R, improved histopathological damage, and reduced the size of cerebral infarction. Combined administration of LV-Malat1-RNAi + Antagomir-211-5p reversed these effects above. In short, our data suggest that LncRNA-Malat is involved in the occurrence and development of cerebral ischemia reperfusion injury by acting on miR-211-5p and is then regulating the expression of COX-2., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Pancreatic cancer is a highly malignant cancer of the digestive tract. Studies have shown that in some types of cancer, a high level of microRNA-194-5p (miR-194-5p) is beneficial for controlling tumor progression, while in other cancers it plays a completely opposite role. However, how miR-194-5p affects anti-tumor immunity of pancreatic cancer remains unclear. In this study, we found that high expression of miR-194-5p in human pancreatic cancer patients is associated with a better survival rate, while increased expression of programmed cell death ligand 1 (PD-L1) in human pancreatic cancer patients is associated with a worse survival rate. In pancreatic cancer, the expression level of PD-L1 is negatively correlated with the expression level of miR-194-5p, and we identified that PD-L1 was target gene of miR-194-5p. In addition, we found that overexpression of miR-194-5p inhibited the migration, invasion and proliferation of pancreatic cancer cells in vitro. The orthotopic mouse model of pancreatic cancer shown that miR-194-5p suppressed the progression of pancreatic cancer, promoted the infiltration of CD8 + T cells in tumor immune microenvironments, and enhanced the IFN-γ production of CD8 + T cells. Consistently, the co-culture experiments showed that overexpression of miR-194-5p in tumor cell enhanced IFN-γ production by CD8 + T cells. In conclusion, miR-194-5p may serve as a novel immunotherapeutic target for pancreatic ductal adenocarcinoma (PDAC) by inhibiting the expression of PD-L1, and play important roles in inhibiting the progression of pancreatic cancer and boosting the anti-tumor effect of CD8 + T cells., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Endothelial cell proliferation disorder caused by vascular injury seems to be one of the causes of atherosclerosis, which is the pathological basis of coronary heart disease. The role of STAT3 in the regulation of microRNAs and endothelial dysfunction in atherosclerosis is unclear. STAT3 can be activated by cytokine IL-6 and up regulate the expression of CX3CL1. In addition, microRNA-15a-5p (miR-15a-5p) inhibited the transcription of CX3CL1, the proliferation of vascular endothelial cells and the proliferation of STAT3 regulated vascular endothelial cells. STAT3 positively regulates the expression of CX3CL1, and then down-regulates the inhibition of CX3CL1 by over-expression of miR-15a-5p, thus forming an elimination feedback loop to control the proliferation of HUVECs and affect the progression of atherosclerosis. In conclusion, miR-15a-5p may be the therapeutic target of the pathological basis of coronary atherosclerosis., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

The present study was to investigate the role of microRNA (miR)-211-5p on cerebral ischemia-reperfusion injury (CIRI) and clarify its underlying mechanisms. Middle cerebral artery occlusion/reperfusion (MCAO/R) was operated on male Sprague Dawley (SD) rats, oxygen-glucose deprivation/reperfusion (OGD/R) was conducted on pheochromocytoma-12 (PC12) cells. Here, we found that miR-211-5p and Cyclooxygenase (COX2) expressions were altered in the plasma, cortex and hippocampus of MCAO/R-treated rats, as well as in the OGD/R-treaded PC12 cells. In vivo, overexpression of miR-211-5p resulted in decrease of infarct volumes, neurological deficit scores and histopathological damage. In vitro, miR-211-5p overexpression significantly decreased cell apoptosis and Lactate dehydrogenase (LDH) release rate, increased cell viability. Furthermore, our data showed that miR-211-5p overexpression markedly reduced the expressions of COX2 mRNA and protein, and the contents of Prostaglandin D2 (PGD2), PGE2, tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β). In addition, inhibition of COX2 significantly rescued the effects of miR-211-5p inhibitor. At last, dual luciferase experimental data showed that miR-211-5p regulated the mRNA stability of COX2 by directly binding to the 3'-untranslated region (3'-UTR) of COX2. In conclusion, our data suggested the neuroprotective effects of miR-211-5p on CIRI by targeting COX2., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Although many methods and new therapeutic drugs have been developed, the overall survival rate and long-term survival rate of patients with gastric cancer (GC) are still not satisfactory. In this study, we investigated the effects of microRNA miR-133a-3p and transcription factor FOXP3 on proliferation and autophagy of GC cells and their interactions. Our results showed that knockdown of FOXP3 increased the proliferation and autophagy of GC cells. The relationship between FOXP3 and autophagy has not been reported previously. In addition, FOXP3 could directly bind the promoter region of TP53 and inhibit its expression. miR-133a-3p increased the proliferation and autophagy via decreasing the protein level of FOXP3 by targeting its 3'-UTR. Our research provides new insights into the development of GC and provides new ideas and theoretical basis for the clinical treatment of GC and the development of new drug targets., (© 2020 Wiley Periodicals, Inc.)

Accumulating evidences indicate that 3'UTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that acvr1b gene 3'UTR (acv3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of acv3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that acv3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in acv3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of acv3UTR. The positive correlation of acv3UTR and YAP1 expression, and the negative correlation of acv3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to acv3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of acv3UTR transcription in GC tumorigenesis, and indicates a correlation between 3'UTR trans-regulatory effect and GC development.

Long intergenic non-coding RNA No.668 (LINC00668) is implicated in the development of various malignancies. However, the role of LINC00668 and underlying mechanism in colorectal cancer (CRC) remains totally unknown. The expression pattern of LINC00668 in CRC cells were determined by qRT-PCR. CCK-8, EdU incorporation, flow cytometry, Transwell, and wound-healing assays were run to evaluate the functions of LINC00668 in CRC cells. Bioinformatics analyses were used to identify the LINC00668-specific binding with miRNAs that were screened by RNA pull-down. RNA immunoprecipitation and luciferase gene report assay were performed to confirm the interaction between miR-188-5p and LINC00668 in CRC cells. LINC00668 was significantly upregulated in CRC tissues and cells. Knockdown of LINC00668 suppressed cell proliferation and migration potential and induced cell apoptosis, but inhibition of miR-188-5p which was predicted to bind with LINC00668 reversed these effects. Furthermore, USP47 was a direct target of miR-188-5p, and overexpression of USP47 attenuated LINC00668 knockdown-induced tumor suppressive effects in CRC cells. Conclusively, our findings demonstrated that lncRNA LINC00668 acted as an oncogenic role in CRC cells by sponging miR-188-5p and upregulating USP47 and may represent a potential marker for CRC patients., (Copyright © 2019 Elsevier B.V. All rights reserved.)

miR-21 is aberrantly expressed, and plays a role in various types of tumors and many other diseases. However, the mechanism of miR-21 in LPS-induced septic shock is still unclear. In this study, we investigated the mechanism of miR-21 in LPS-induced pyroptosis and septic shock. Here, we show that miR-21 deficiency inhibited NLRP3, ASC, and caspase-1 expression, as well as inflammasome activation in myeloid cells from both mice and humans. We found that the NF-κB pathway was regulated by miR-21, and that A20 was a direct target of miR-21. Furthermore, miR-21 deficiency inhibited the ASC pyroptosome, which restrained caspase-1 activation and GSDMD cleavage, thereby preventing LPS-induced pyroptosis and septic shock. miR-21 deficiency resulted in an increase in A20, which led to decreased IL-1β production and caspase-1 activation. Caspase-1-mediated GSDMD cleavage was consequently decreased, which prevented pyroptosis in LPS-induced sepsis in mice. Our results demonstrate that miR-21 is a critical positive regulator of the NF-κB pathway and NLRP3 inflammasomes in pyroptosis and septic shock via A20. In addition, by analyzing published miRNA expression profiles in the Gene Expression Omnibus database, we found that the miR-21 levels in peripheral blood from patients with septic shock were elevated. Thus, miR-21 may serve as a potential treatment target in patients with septic shock.

Background: Bone-marrow derived mesenchymal stem cells (BM-MSCs) implantation effectively restored rats' erectile dysfunction (ED). Long noncoding RNA (LncRNA)-myocardial infarction-associated transcript (MIAT) has been reported to play an important role in regulating endothelial cells (ECs) function via vascular endothelial growth factor (VEGF) that induced BM-MSCs differentiation into ECs. However, the molecular functions and biological roles of lncRNA MIAT in ED remained unclear., Methods: The rat model of ED was established. Quantitative real-time PCR (qRT-PCR) and western blotting were used to detect the expression of lncRNA MIAT, von Willebrand factor (vWF), vascular endothelial cadherin (VE-cadherin), endothelial NO synthase (eNOS) and VEGF following BM-MSCs transfection. Erectile function was evaluated by intra-cavernous pressure/mean artery pressure (ICP/MAP). Furthermore, RNA immunoprecipitation (RIP) assay and RNA pull down as well as luciferase reporter assay were carried out to examine the interaction among lncRNA MIAT, miR-200a and VEGF., Results: BM-MSCs restored ED by upregulating lncRNA MIAT. LncRNA MIAT was upregulated in a time-dependent manner during BM-MSCs differentiation into ECs. LncRNA MIAT regulated VEGF via targeting miR-200a, thereby promoting BM-MSCs differentiation into ECs. LncRNA MIAT knockdown in vivo abolished the effect of BM-MSCs on ED., Conclusion: LncRNA MIAT promoted BM-MSCs differentiation into ECs and restored ED via miR-200a., (Copyright © 2018 Elsevier GmbH. All rights reserved.)

Breast cancer is the leading cause of cancer death in women worldwide which is closely related to metastasis. Our previous study has shown that MRTF-A promote the migration of MDA-MB-231 cells and WDR1 promotes breast cancer cell migration. But the exact molecular mechanism on metastasis is still not fully understood, we now report that WDR1 enhanced the effect of MRTF-A induced-MDA-MB-231 cell migration by promoting the expression of the EMT markers and migration markers via RhoA-MRTF-A signaling pathway. Importantly, WDR1 promoted the nuclear importion of MRTF-A by affecting the expression of nuclear transport protein importin. But WDR1 did not affect the expression of MRTF-A. Interestingly, MRTF-A promoted the expression of miR-206 via its promoter CArG box but miR-206 inhibits the migration of breast cancer cells through suppressing the expression of WDR1 and MRTF-A via targeted their 3'UTR. Our data thus provide important and novel insights into MRTF-A-miR-206-WDR1 form feedback loop to regulate breast cancer cell migration., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Epithelial-mesenchymal transition (EMT) plays an important role in breast cancer cell metastasis. Both (megakaryoblastic leukemia)/myocardin-like 1 (MKL-1) and Signal transducer and activator of transcription 3 (STAT3) have been implicated in the control of cellular metabolism, survival and growth. Our previous study has shown that cooperativity of MKL-1 and STAT3 promoted breast cancer cell migration. Herein, we demonstrate a requirement for MKL-1 and STAT3 in miRNA-mediated cellular EMT to affect breast cancer cell migration. Here we show that cooperativity of MKL-1 and STAT3 promoted the EMT of MCF-7 cells. Importantly, MKL-1 and STAT3 promoted the expression of Vimentin via its promoter CArG box. Interestingly, miR-93-5p inhibits the EMT of breast cancer cells through suppressing the expression of MKL-1 and STAT3 via targeted their 3'UTR. These results demonstrated a novel pathway through which miR-93-5p regulates MKL-1 and STAT3 to affect EMT controlling breast cancer cell migration., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Radon has long been recognized as a human carcinogen leading to lung cancer, but the underlying mechanisms remain obscure. Recent studies have shown that the let-7 microRNA and K-ras play an important role in the development of various cancers. However, the exact role between let-7 and K-ras in radon induced lung damage has not been explored so far. In the present study, wistar rats and human bronchial epithelial (HBE) cells were long-term exposed to radon, and then alterations in histological pathology of rat lung tissue, ROS, antioxidant enzymes activities and clonogenic formation in HBE cells, as well as changes in let-7 and K-ras expression were determined to observe the adverse effects induced by radon. The results showed that long-term exposure to radon produced severe lung damage in rats, significantly increased ROS production and clonogenic formation ratios and decreased SOD activities in HBE cells. In addition, an obvious down-regulation of let-7 and up-regulation of K-ras were also revealed both in mRNA and in protein level in lung tissue of rats and HBE cells exposed to radon. Furthermore, a significant down-regulation of K-ras was then confirmed in both let-7b-3p and let-7a-2-3p transfected HBE cells. Taken together, the present results propose an involvement of let-7 microRNA and K-ras in radon induced lung damage both in vivo and in vitro, which may thus be of potential value in early diagnosis and therapy of radon-induced lung tumorgenesis., (Copyright © 2015 Elsevier B.V. All rights reserved.)

MicroRNAs (miRNAs) are known to function as negative gene regulators. Recently, miRNAs have been shown to regulate immunity processes; however, the mechanism is unclear. The role of microRNA-214 (miR-214) in dendritic cell (DC) maturation has not been investigated. We found that the miR-214 level was correlated with the maturation of DCs and inflammatory cytokine secretion, as depressed miR-214 levels induced DC tolerance. We also identified β-catenin as a target gene of miR-214 and demonstrated its association with Treg cell differentiation. MiR-214 regulates gene expression by binding to the 3'UTR of β-catenin. The results suggest that β-catenin is a critical regulator of tolerance in DCs via miR-214. The expression of miR-214 could be a potential therapeutic strategy in organ transplantation or autoimmunity patients.