CircVDAC3 sequesters microRNA-592 and elevates EIF4E3 expression to inhibit the progression of gastric cancer.

BACKGROUND: Accumulating evidence has shown that circular RNAs (circRNAs) are involved in gastric cancer (GC) tumorigenesis. However, specific functional circRNAs in GC remain to be discovered, and their underlying mechanisms remain to be elucidated. METHODS: CircRNAs that were differentially expressed between GC tissues and controls were analyzed using a circRNA microarray dataset. The expression of circVDAC3 in GC was determined using quantitative real-time PCR (qRT-PCR), and the structural features of circVDAC3 were validated. Cell function assays and animal experiments were conducted to explore the effects of circVDAC3 on GC. Finally, bioinformatics analysis, fluorescent in situ hybridization, and dual luciferase assays were used to analyze the downstream mechanisms of circVDAC3. RESULTS: Our results showed that circVDAC3 was downregulated in GC and inhibited the proliferation and metastasis of GC cells. Mechanistically, circVDAC3 acts as a competing endogenous RNA (ceRNA) of miR-592 and deregulates the repression of EIF4E3 by miR-592. EIF4E3 is downregulated in GC and overexpression of miR-592 or knockdown of EIF4E3 in circVDAC3-overexpressing cells weakens the anticancer effect of circVDAC3. CONCLUSION: Our study provides evidence that circVDAC3 affects the growth and metastasis of GC cells via the circVDAC3/miR-592/EIF4E3 axis. Our findings offer valuable insights into the mechanisms underlying GC tumorigenesis and suggest novel therapeutic strategies.

The clinical diagnostic value of plasma miR-592 and miR-217-3p levels in retinoblastoma.

Background: This study was designed to investigate the abnormal expression of plasma miR-592 and miR-217-3p in retinoblastoma (Rb) and explore the clinical diagnostic value of their expression levels for Rb. Methods: The 100 Rb patients who came to Nanchang Hongdu Hospital of Traditional Chinese Medicine from January 2018 to January 2019 were selected as the Rb group, and 100 healthy patients who came to the physical examination centre during the same period were selected as the control group. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression levels of plasma miR-592 and miR-217-3p in all subjects; analyse the relationship between plasma miR-592 and miR-217-3p levels and the clinicopathological characteristics of Rb. Pearson correlation analysis evaluated the relationship between plasma miR-592 and miR-217-3p levels and overall survival. Results: Plasma levels of miR-592 and miR-217-3p in the Rb group were significantly higher than those in the control group (p<0.0001), and the expression of miR-592 was significantly correlated with family genetic history (p 0.0001), tumour bias (p=0.0081), lymph node metastasis (p=0.0048) and pathological grade (p=0.0025), and the expression of miR-217-3p was significantly related to family genetic history (p 0.0001), optic nerve infiltration (p 0.0001), lymph node metastasis (p=0.0090), and pathological grade (p 0.0001). The high expression of miR-592 and miR-217-3p presents a more serious pathological manifestation of Rb, and the overall survival of patients is significantly shortened with the increase of miR-592 (r=-0.2276, p=0.0052) and miR-217-3p levels (r=-0.6461, p 0.0001). Conclusions: and miR-217-3p are highly expressed in the plasma of Rb patients, and their elevated levels present severe pathological manifestations of Rb and shortened overall survival, which is expected to become biomarkers for clinical diagnosis of Rb.

Roles of miR-592-3p and Its Target Gene, TMEFF1, in the Nucleus Accumbens During Incubation of Morphine Craving.

BACKGROUND: Prolonged forced abstinence from morphine can increase cue-induced cravings for the drug, contributing to a persistent vulnerability to relapse. Previous studies have identified the implications of aberrant microRNA (miRNA) regulation in the pathogenesis of morphine addiction, but the changes in miRNA expression during the incubation of morphine craving are still unknown. METHODS: Nucleus accumbens (NAc)-specific altered miRNA transcriptomics was determined in a mouse model of cue-induced incubation of morphine craving following a next-generation sequencing method and verified by RT-qPCR. Bioinformatics analysis was performed to predict the target gene of selected miRNA, and the protein expression of the target gene was detected by western blot. A dual-luciferase assay was performed to confirm the binding sites, and gain- and loss-of-function strategy was applied to understand the mechanism of miRNA and its target gene. RESULTS: The miR-592-3p observed to be downregulated in the NAc core was linked to the incubation of morphine craving, and a dual-luciferase assay was performed to confirm the binding sites of miR-592-3p in its target gene, tomoregulin-1 (TMEFF1). Also, gain- and loss-of-function analyses revealed that the inhibition of miR-592-3p expression in the NAc core negatively regulated TMEFF1 expression, thereby enhancing the incubation of morphine craving; however, the overexpression of miR-592-3p in the NAc core resulted in a decreased expression of TMEFF1, thereby reducing the incubation of morphine craving. CONCLUSION: Our findings demonstrated that miR-592-3p can improve the incubation of morphine craving by targeting TMEFF1, and thus, it holds a therapeutic potential to inhibit opioid craving.

MicroRNA-592 serves as a novel tumor suppressor in Uveal melanoma: bioinformatics analysis and in vitro cell function verification.

Uveal melanoma (UVM), one common eye tumor in adults, is related with a high risk of metastasis and poor prognosis. Studies have shown that many miRNAs are abnormally expressed in UVM tissues, and play an important regulatory role in the cell proliferation, invasion, and metastasis of UVM. Therefore, it is of great significance to analyze the expression characteristics of microRNAs (miRNAs) in UVM and clarify the role of miRNA in the tumorigenesis and development of UVM. In this study, we firstly downloaded and analyzed miRNA expression data of UVM tissues in TCGA (The Cancer Genome Atlas) database to select the differential expressed miRNAs in different clinical stages (IIA, IIB, IIIA, IIIB, IV). Compared with other stages, microRNA-592 (miR-592) was up-regulated in stage IV UVM patients. Then we used several bioinformatics tools including miRbase, miRDB, RNA22 and TargetScan, and found that it was be conserved in different species. Cell viability was determined by Cell Counting Kit-8. The proliferation and invasion of MUM-2B and C819 cells was measured using Edu assay and Transwell assay. We found that silencing miR-592 enhanced the progression of UVM cells, while miR592 overexpression inhibited the cell growth and invasion. The target genes of miR-592 were predicted by three webservers (miRDB, RNA22, and TargetScan), and verified by Real-Time PCR (qPCR). This is the first study to explore the role of miR-592 in malignant progression of UVM by bioinformatics and cell experiments. Our study suggests that tumor suppressor miR-592 may function as potential therapeutic target and biomarker for UVM.

Compared with other clinical stages of UVM, miR-592 was found highly expressed in Stage IV.Down-regulating miR-592 can promote the progression of UVM cells, while its overexpression inhibits the cell growth and invasion.STAT1, RBBP4, and DLG4 may be the target genes of miR-592 in UVM.

Increased Expression of miR-7a-5p and miR-592 during Expansion of Rat Dental Pulp Stem Cells and Their Implication in Osteogenic Differentiation.

Dental pulp stem cells (DPSCs) possess strong osteogenic differentiation potential and are promising cell sources in regenerative medicine. However, such differentiation capacity progressively declines during their in vitro expansion. MicroRNAs (miRNAs) play important roles in modulating stem cell differentiation. This study aimed (1) to determine if miR-7a-5p and miR-592 are involved in maintaining and regulating osteogenic differentiation of DPSCs, and (2) to explore their potential regulatory pathways. We found that the expression of miR-7a-5p and miR-592 was significantly upregulated during the expansion of rat DPSCs (rDPSCs). Overexpression of these miRNAs inhibited the osteogenic/odontogenic differentiation of rDPSCs, as evidenced by calcium deposition and osteogenic/odontogenic gene expression. RT-qPCR determined that miR-592 could downregulate heat shock protein B8, whose expression is reduced during the expansion of rDPSCs. Furthermore, RNA-seq and bioinformatics analysis identified significant signaling pathways of miR-7a-5p and miR-592 in regulating osteogenic differentiation, including TNF, MAPK, and PI3K-Akt pathways. We conclude that upregulating miR-7a-5p and miR-592 suppresses the osteogenic differentiation of rDPSCs during their in vitro expansion, likely via TNF, MAPK, and PI3K-Akt pathways. The results may shed light on application of miR-7a-5p and miR-592 for maintaining osteo-differentiation potential in stem cells for bone regeneration and bone-related disease treatment.

[Retracted] miR­592 functions as a tumor suppressor in human non­small cell lung cancer by targeting SOX9.

Following the publication of the above paper, the authors submitted a request to the Editorial Office to publish a corrigendum in light of a concern regarding potential contamination of their cells during the course of performing the experiments; at the same time, it was drawn to the Editors' attention by a concerned reader that certain of the colony­formation assay data shown in Fig. 2C were strikingly similar to data appearing in different form in another article by different authors. Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 37: 297-304, 2017; DOI: 10.3892/or.2016.5275].

A Novel Identified Long Non-coding RNA, lncRNA MEF2C-AS1, Inhibits Cervical Cancer via Regulation of miR-592/RSPO1.

Purpose: Our purpose was to investigate the effect of lncRNA MEF2C antisense RNA 1 (MEF2C-AS1) on cervical cancer and further explore its underlying molecular mechanisms. Methods: The proliferation, migration and invasion of CC cells were determined by counting Kit-8 (CCK-8), colony formation assay, and transwell assays, respectively. qRT-PCR and western blot were conducted to quantitatively detect the expression of lncRNA MEF2C-AS1, miR-592 and R-spondin1 (RSPO1). Kaplan-Meier survival curve from the Cancer Genome Atlas (TCGA) database and the Gene Expression Profiling Interactive Analysis (GEPIA) website was used to describe the overall survival. Bioinformatics analysis was performed to search the downstream target of lncRNA MEF2C-AS1 and miR-592. Luciferase reporter assay was conducted to detect the interaction between lncRNA MEF2C-AS1 and miR-592 or miR-592 and RSPO1. Results: The data from GEPIA website showed that lncRNA MEF2C-AS1 expression was down-regulated in CC tissues and also associated with survival rate of CC patients. Moreover, the results of qRT-PCR also showed lncRNA MEF2C-AS1 was lowly expressed in CC cells. Subsequently, we confirmed that overexpression of lncRNA MEF2C-AS1 inhibited the proliferation, migration and invasion of CC cells. Further research illustrated that lncRNA MEF2C-AS1 was the target of miR-592, and RSPO1 was the downstream target gene of miR-592. Importantly, functional research findings indicated that lncRNA MEF2C-AS1 inhibited CC via suppressing miR-592 by targeting RSPO1. Conclusion: In our study, we demonstrated the functional role of the lncRNA MEF2C-AS1-miR-592-RSPO1 axis in the progression of CC, which provides a latent target for CC treatment.

Aberrant Expression of miR-592 Is Associated with Prognosis and Progression of Renal Cell Carcinoma.

PURPOSE: MicroRNAs have recently reported playing a vital role in the development of cancers. However, the role of miR-592 in renal cell carcinoma (RCC) has not been explored. In this study, the potential role of miR-592 was investigated in RCC. PATIENTS AND METHODS: The expression of miR-592 was evaluated in RCC tissues and cell lines using qRT-PCR assays. The Kaplan-Meier analysis and Cox proportional hazards model analysis was used to analyze the prognostic value of miR-592 in RCC. The effects of miR-592 on cell proliferation, migration, and invasion were determined by cell counting kit-8 (CCK-8) and Transwell assays in vitro. RESULTS: The results showed that miR-592 was significantly increased both in RCC tissues and cell lines. Overexpression of miR-592 was significantly associated with lymph node metastasis, TNM stage, and poor overall survival. And functional studies in two RCC cell lines (786-O and Caki-1) have shown that overexpression of miR-592 promoted cell proliferation, migration, and invasion, while silence of miR-592 inhibited cell proliferation, migration, and invasion. SPRY2 was a direct target of miR-592. CONCLUSION: Overall, overexpression of miR-592 may be a prognostic biomarker and therapeutic strategy for patients with RCC, which is correlated with the progression of RCC.

MiR-592 Promotes Gastric Cancer Proliferation, Migration, and Invasion Through the PI3K/AKT and MAPK/ERK Signaling Pathways by Targeting Spry2.

BACKGROUND/AIMS: Gastric cancer (GC) is one of the most prevalent digestive malignancies. MicroRNAs (miRNAs) are involved in multiple cellular processes, including oncogenesis, and miR-592 itself participates in many malignancies; however, its role in GC remains unknown. In this study, we investigated the expression and molecular mechanisms of miR-592 in GC. METHODS: Quantitative real-time PCR and immunohistochemistry were performed to determine the expression of miR-592 and its putative targets in human tissues and cell lines. Proliferation, migration, and invasion were evaluated by Cell Counting Kit-8, population doubling time, colony formation, Transwell, and wound-healing assays in transfected GC cells in vitro. A dual-luciferase reporter assay was used to determine whether miR-592 could directly bind its target. A tumorigenesis assay was used to study whether miR-592 affected GC growth in vivo. Proteins involved in signaling pathways and the epithelial-mesenchymal transition (EMT) were detected with western blot. RESULTS: The ectopic expression of miR-592 promoted GC proliferation, migration, and invasion in vitro and facilitated tumorigenesis in vivo. Spry2 was a direct target of miR-592 and Spry2 overexpression partially counteracted the effects of miR-592. miR-592 induced the EMT and promoted its progression in GC via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2. CONCLUSIONS: Overexpression of miR-592 promotes GC proliferation, migration, and invasion and induces the EMT via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2, suggesting a potential therapeutic target for GC.

miR-592 induces apoptotic cell death in human U251 cells / 中国神经精神疾病杂志

Objective To investigate the role of miR-592 in the Glioma.Methods We first analyzed the expression of miR-592 in Glioma tissues from patients by quantitative PCR.We transfected U251 cells with miR-592 mimics and then detected the growth of cells by MTT assay.We performed dual-luciferase reporter assay and western blot assay to examine whether Runx2 was the direct target of miR-592 in U251 cells.In order to test whether Runx2 was the functional target of miR-592,we determined the cell growth curve by down-regulating the level of Runx2.Moreover,we also detected the apoptosis of U251 after Runx2 knockdown.Results The expression of miR-592 was significantly reduced in glioma tissues (t=2.752,P--0.013).Over-expression miR-592 remarkably increased the apoptotic rate of U251 cells compared with the control group (t=2.127,P=0.031;t=2.284,P=0.026).Flow cytometry analysis showed that MiR-592 significantly promoted apoptotic cell death of U251 cells Apoptosis rate was 7.2％±0.68％ in miR-592 group and 17.47％±1.45％ in control group (t=3.294,P=0.007).The results of double luciferase assay and Western blot assay showed that miR-592 directly targeted the 3'Runx2 of-UTR to inhibit the level of Runx2 protein.The effect of down-regulation of Runx2 on the growth of U251 cells was detected,the results showed that growth was significantly slower in the cells transfected with Runx2 siRNA than in those without Runx2 siRNA (t=3.124,P=0.O11).Detection of cycle by flow cytometry showed that runx2 down-regulated the apoptosis rate of U251 cells.Tumor growth curve showed that overexpression of miR-592 significantly inhibited tumor growth and the down regulation of Runx2 expresssion also significantly inhibited tumor growth.Conclusion miR-592 suppresses the growth and promotes the apoptotic rate of U251 cells by targeting Runx2.

AK048794 maintains the mouse embryonic stem cell pluripotency by functioning as an miRNA sponge for miR-592.

MiR-592 has been identified as a neural-enriched microRNA, plays an important role in mNPCs differentiation, could induce astrogliogenesis differentiation arrest or/and enhance neurogenesis in vitro Previous studies showed that long noncoding RNAs (lncRNAs) were involved in the neuronal development and activity. To investigate the role of miR-592 in neurogenesis, we described the expression profile of lncRNAs in miR-592 knockout mouse embryonic stem cells (mESCs) and the corresponding normal mESCs by microarray. By the microarray analysis and luciferase reporter assays, we demonstrated that lncRNA - AK048794, regulated by transcription factor GATA1, functioned as a competing endogenous RNA (ceRNA) for miR-592 and led to the de-repression of its endogenous target FAM91A1, which is involved in mESC pluripotency maintenance. Taken together, these observations imply that AK048794 modulated the expression of multiple genes involved in mESC pluripotency maintenance by acting as a ceRNA for miR-592, which may build up the link between the regulatory miRNA network and mESC pluripotency.

An oncogenic role of miR-592 in tumorigenesis of human colorectal cancer by targeting Forkhead Box O3A (FoxO3A).

OBJECTIVE: A microRNA (miRNA) that functionally downregulates the expression of tumor suppressors can be defined as an oncomir. Here, we interrogate the biological significance of miR-592 in colorectal cancer (CRC). RESEARCH DESIGN AND METHODS: The expression of miR-592 in CRC tissues and cell lines was ascertained by qRT-PCR assay, and the expression of its target gene was determined by immunohistochemistry staining. The oncogenic role of miR-592 was assessed in terms of cell proliferation, migration, and clonogenicity in vitro, whereas the tumorigenicity was assessed by inhibiting endogenous miR-592 in CRC cells in vivo. RESULTS: A striking upregulation of miR-592 was observed in CRC tissues and cell lines compared to the matched adjacent non-tumor tissues and normal colon cells. Importantly, Forkhead Box O3A (FoxO3A) was identified as a novel target of miR-592. miR-592 inhibitor exhibited a significant reduction of migration, proliferation, and clonogenicity in CRC cells. These cells also displayed a decreased tumorigenicity in SCID mice relative to the control cells. CONCLUSION: These data suggest that miR-592 may promote the progression and metastasis, in part, by targeting FoxO3A in CRC. miR-592 may be a novel target for CRC treatment and antagomir-592 may inhibit the proliferation and metastasis of CRC cells.

miR-592/WSB1/HIF-1α axis inhibits glycolytic metabolism to decrease hepatocellular carcinoma growth.

Hepatocellular carcinoma (HCC) cells rapidly switch their energy source from oxidative phosphorylation to glycolytic metabolism in order to efficiently proliferate. However, the molecular mechanisms responsible for this switch remain unclear. In this study, we found that miR-592 was frequently downregulated in human HCC tissues and cell lines, and its downregulation was closely correlated with aggressive clinicopathological features and poor prognosis of HCC patients. Overexpression of miR-592 inhibited aerobic glycolysis and proliferation in HCC cells in vitro. Conversely, knockdown of miR-592 promoted HCC growth in both subcutaneous injection and orthotopic liver tumor implantation models in vivo. Mechanistically, miR-592 downregulation in human HCCs was correlated with an upregulation of WD repeat and SOCS box containing 1 (WSB1). We further showed that miR-592 directly binds to the 3'-UTR of the WSB1 gene, thus disrupting hypoxia inducible factor-1α (HIF-1α) protein stabilization. In turn, overexpression of WSB1 in HCC cells rescued decreased HIF-1α expression, glucose uptake, and HCC growth induced by miR-592. Collectively, our clinical data and functional studies suggest that miR-592 is a new robust inhibitor of the Warburg effect and a promising therapeutic target for HCC treatment.

miRNA-592 is downregulated and may target LHCGR in polycystic ovary syndrome patients.

The polycystic ovary syndrome (PCOS) is an endocrine disorder mainly associated with infertility. Abnormal regulation of relevant genes is required for follicular development in PCOS. In the current study, the expression of serum miRNAs of PCOS patients was explored using miRNA array followed by qRT-PCR assays. The circulating level of miR-592 was significantly down-regulated in PCOS patients in comparison with healthy controls. Furthermore, we found that miR-592 was inversely correlated with the level of luteinizing hormone/chorionic gonadotropin receptor (LHCGR). Computational analysis predicted that miR-592 interacts with the LHCGR mRNA via binding to a site located in the 3'UTR region. Using a luciferase-based reporter assay we found that miR-592 directly targeted the LHCGR. In KGN cell line, miR-592 overexpression inhibited cell viability and the transition of phase G1 to phase S. Knocking down of LHCGR inhibited cell viability and cell cycle progression in KGN cells, and LHCGR co-transfection reversed the inhibitory effect of miR-592. These results shed new light on the diagnosis and treatment of PCOS syndrome.

MiR-592 represses FOXO3 expression and promotes the proliferation of prostate cancer cells.

Prostate cancer (PC) is a serious health problem all over the world. Cell proliferation plays a major role in the tumorigenesis of PC. It is reported that microRNAs (miRNAs) played crucial roles in the regulation of cell proliferation. However, the underlying mechanism of miRNAs in PC has not been intensively investigated. In the present study, the effect of miR-592 on the cell proliferation of PC was investigated. The results showed that miR-592 was significantly upregulated in PC cell and PC tissues. To investigate the biological roles of miR-592, we induced either the up- or downregulation of miR-592 expression by transfecting DU145 PC cells with miR-592 mimics or miR-592 inhibitor. Our results demonstrated that the upregulation of miR-592promoted cell growth, while miR-592 inhibitor showed the opposite effect. Further experiment revealed that miR-592 repressed the expression of FOXO3 by directly targeting the 3'UTR of the FOXO3 transcript, which resulted in upregulating of the expression of cyclin D1 and downregulating of the expression of p21. In sum, our data indicated a novel aspect of the miR-592 in the molecular etiology of PC.

MiR-592 inhibited cell proliferation of human colorectal cancer cells by suppressing of CCND3 expression.

Accumulating evidence shows that microRNA (miRNA) is frequently associated with multiple kinds of human cancers, including colorectal cancer (CRC). Previous studies have shown that miR-592 play critical roles in cancer cell biological processes. However, the function of miR-592 in CRC remains largely unknown. In the present study, we investigated the miR-592's role in cell proliferation of colorectal cancer. MiR-592 expression was markedly down-regulated in CRC tissues and CRC cells. Overexpression of miR-592 reduced the proliferation and anchorage-independent growth of CRC cells. Furthermore, bioinformatics analysis further revealed CCND3, a putative tumor promoter, was found to be a potential target of miR-592 in CRC. The dual-luciferase reporter gene assay results showed that CCND3 was a direct target of miR-592. Ectopic expression of miR-592 led to down-regulation of CCND3 protein, which resulted in the down-regulation of phosphorylated retinoblastoma (p-Rb). In functional assays, CCND3-silenced in miR-592-in-transfected SW48 cells have positive effect to suppress cell proliferation, suggesting that direct CCND3 suppression is required for miR-592-induced cell proliferation of CRC. We conclude that miR-592 can regulate CCND3 and function as a tumor suppressor in CRC. Therefore, miR-592 represents a potential anti-onco-miR and serves as a useful therapeutic agent for miRNA-based CRC therapy.

Up-regulation of miR-592 correlates with tumor progression and poor prognosis in patients with colorectal cancer.

miR-592, as a potential biomarker, has been linked to several cancers. However, the expression level and prognostic value of miR-592 in CRC have not been elucidated. In this study, we detected the miR-592 expression in CRC serum, tumor tissues, adjacent non-tumor tissues (NATs) and four colorectal cancer cell lines by RT-PCR. Our data proved that miR-592 expression was up-regulated in clinical CRC serum and tissues (P<0.05). Serum or tissue miR-592 in CRC metastatic patients also maintained a high level, compared to that in non-metastatic CRC patients (P<0.05). After radical surgery, postoperative serum miR-592 level in CRC patients significantly decreased (P<0.05). Our clinicopathological analysis revealed that high miR-592 was significant associated with the tumor size (P=0.008), TNM stage (P=0.026), distant metastasis (P=0.004) and preoperative CEA level (P=0.022), which led to a shorter overall survival rate in CRC patients (P=0.032). Furthermore, we designed and transfected miR-592 mimics or inhibitors into the corresponding CRC lines, and our experiments in vitro demonstrated that miR-592 could promote cell proliferation, wound healing and invasion ability of CRC cells (P<0.05), while miR-592 did not influence the CRC cell apoptosis (P>0.05). All these results suggested that miR-592 functioned as a novel and potential carcinogen-initiated and metastasis-related biomarker in CRC, and down-regulation of miR-592 might be considered as a potentially significant molecular treatment strategy for CRC patients.

MicroRNA-592 targets DEK oncogene and suppresses cell growth in the hepatocellular carcinoma cell line HepG2.

MicroRNAs (miRNAs) are classes of small, non-coding RNAs that regulate the translation of target mRNA transcripts. In this study, we demonstrated that miR-592 was downregulated in human hepatocellular carcinoma (HCC) and could suppress growth of the human HCC cell line HepG2. A tumor oncogene, DEK, was identified as a direct target of miR-592. Luciferase report assay indicated miR-592 regulates DEK expression though bind to its 3'UTR. Furthermore, knockdown of DEK also suppressed cell proliferation of HepG2 cells, which was consist with miR-592. At last, we suggested that DEK was upregulated in HCC tissues inversely with miR-592. These results demonstrated that miR-592 targets DEK transcript and suppresses HCC cell growth, and may provide potential therapeutic target in human HCC.