Circular RNA-0072309 has antitumor influences in Hep3B cell line by targeting microRNA-665.

Liver cancer is a malignant tumor that occurs in the liver and has a high mortality rate. We strived to detect the role and mechanism of circRNA-0072309 in liver cancer. Hep3B cell line was transfected with pc-circ and si-circ for viability, colony formation, apoptosis, migration, and invasion tests, which were individually performed by CCK-8, colony formation detection, flow cytometry assay, migration and invasion assays. What is more, the luciferase reporter assay was conducted to determine the target relationship between the circRNA-0072309 and microRNA (miR)-665. The expression of circRNA-0072309 was examined by qRT-PCR. The expression of proteins was examined via western blot. CircRNA-0072309 was lowly expressed in liver cancer tissues and positively associated with 5-year survival rate. The viability, colony formation, invasive and migratory ability were inhibited by abundant circRNA-0072309, which promoted cell apoptosis on the contrary. CircRNA-0072309 knockdown induced opposite effects, but could not affect apoptosis. Overexpressed miR-665 in tumor tissues was targeted and negatively controlled by circRNA-0072309. The PI3K/AKT and Wnt/ß-catenin pathways were inhibited by abundant circRNA-0072309. miR-665 overexpression disturbed those effects derived from pc-circ. The circRNA-0072309 had antitumor influences in Hep3B cell line through targeting miR-665 relying on the deactivation of PI3K/AKT and Wnt/ß-catenin pathways.

[Retracted] MicroRNA­21 increases cell viability and suppresses cellular apoptosis in non­small cell lung cancer by regulating the PI3K/Akt signaling pathway.

Following the publication of this paper, the authors have contacted the Editorial Office to request that their article be retracted. The reason for this retraction is an inability to be able to replicate certain of their previous results, and also disagreements among the authors as to the interpretation of some of the data. Following further discussion, all authors and the Editor of Molecular Medicine Reports are in agreement that the paper should be retracted; moreover, the authors apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 16: 6506­6511, 2017; DOI: 10.3892/mmr.2017.7440].

Retraction: Hsa_circ_0003645 shows an oncogenic role by sponging microRNA-1299 in hepatocellular carcinoma cells.

Retraction: "Hsa_circ_0003645 shows an oncogenic role by sponging microRNA-1299 in hepatocellular carcinoma cells", by Qiuyun Yu, Jinhua Dai, Ming Shu, Journal of Clinical Laboratory Analysis, 2020, e23249 (https://doi.org/10.1002/jcla.23249). The above article, published online on 28 February 2020 in Early View in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor-in-Chief Junming Guo, and John Wiley & Sons Ltd. The retraction has been agreed because the data and figures, including figure 7A, that the authors present in the paper are flawed. The authors' original data are not available. The conclusions drawn from the data and figures are unreliable.

circCDYL/microRNA-105-5p participates in modulating growth and migration of colon cancer cells.

Circular RNA-microRNA (circRNA-miR) node has recently been found to modulate cancer process. Here, we investigated whether circCDYL and miR-150-5p exerted biological function in colon cancer cells. Colon cancer tissues were collected and subjected to qRT-PCR assay for circCDYL and miR-150-5p. SW480 and SW620 cells were forced to overexpress circCDYL and miR-150-5p before subjected to viability, colony formation, apoptosis, migration, invasion and protein (associated with proliferation, apoptosis and signaling pathways) assays. To confirm the combined function, the cells were transfected to simultaneously overexpress circCDYL and miR-150-5p. We found circCDYL was generally decreased while miR-150-5p was increased in colon cancer tissues in parallel with the para-carcinoma tissues. In circCDYL-transfected SW480 and SW620 cells, circCDYL decreased viability and promoted apoptosis with down-regulation of c-Myc and cyclin D1, up-regulation of p53, and cleavage of caspase-3 and PARP. Besides, migration and invasion behaviors were impeded. By contrast, miR-150-5p showed a carcinogenesis. However, suppressive role of circCDYL in cellular growth and migration was restrained in the cells simultaneously transfected with circCDYL and miR-150-5p, which was companied by down-regulation of PTEN and phosphorylation of PI3K, AKT, JAK2 and STAT5. circCDYL overexpression repressed cellular growth and migration via repressing miR-150-5p in colon cancer cells.

Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5.

Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.

microRNA-29a functions as a tumor suppressor in nasopharyngeal carcinoma 5-8F cells through targeting VEGF.

OBJECTIVES: microRNA-29 (miR-29) family miRNAs have been mentioned as tumor suppressive genes in several human cancers. The purpose of this study was to investigate the function of miR-29a in nasopharyngeal carcinoma (NPC) cells. MATERIALS AND METHODS: Human NPC cell line 5-8F was transfected with mimic, inhibitor or scrambled controls specific for miR-29a. Subsequently, cell viability, migration, apoptosis and expression changes of VEGF were assessed by trypan blue staining, MTT assay, transwell assay, flow cytometry, Western blot and RT-qPCR. TargetScan online database was used to predict the targets of miR-29a, and luciferase reporter assay was carried out for testing the targeting relationship between VEGF and miR-29a. Western blot analysis was performed to determine the expression changes of core proteins in PI3K/AKT and JAK/STAT pathways. RESULTS: Overexpression of miR-29a suppressed 5-8F cells viability and relative migration, but increased apoptotic cell rate. Consistently, Bcl-2 was downregulated, Bax was upregulated, and caspase-3 and -9 were cleaved by miR-29a overexpression. VEGF was a target gene of miR-29a. Besides, VEGF silence exerted similar effects like miR-29a, as the viability and migration were repressed and apoptosis was induced. Finally, we found that PI3K/AKT and JAK/STAT pathways were deactivated by miR-29a or VEGF silence. CONCLUSION: These findings highlighted the tumor suppressive effects of miR-29a on NPC cells, as its overexpression inhibited 5-8F cells viability, migration, and induced apoptosis. miR-29a exerted tumor suppressive functions might be via targeting VEGF and deactivating PI3K/AKT and JAK/STAT pathways.

MicroRNA-16 inhibits cell proliferation and migration by targeting heat shock protein 70 in heat-denatured dermal fibroblasts.

BACKGROUND/AIMS: This study aimed to investigate the precise mechanism and function of miR-16 in heat-denatured primary human dermal fibroblasts. METHODS: Primary human dermal fibroblasts were separated from normal human skin samples. Under heat stress, the levels of miR-16 and heat shock protein 70 (HSP70) were detected in primary human dermal fibroblasts by quantitative real-time polymerase chain reaction (qRT-PCR). Next, heat-denatured cells were transfected with synthetic scrambled negative control (NC) RNA (NC group), miR-16 mimics, miR-16 inhibitor or miR-16 inhibitor accompanied by small interfering RNA targeting HSP70, then the mRNA level of HSP70 was detected by qRT-PCR, cell proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and AlamarBlue assay, cell migration was examined by Transwell assay and cell apoptosis was assessed by transferase dUTP (deoxyuridine triphosphate) nick end labeling (TUNEL) assay. In addition, cell apoptosis-related proteins, Bax and Bcl-2, were detected by Western blotting. RESULTS: Heat stress significantly reduced miR-16 level and increased the mRNA level of HSP70 compared with untreated cells (p < 0.05). Overexpressed miR-16 reduced the mRNA level of HSP70, suppressed cell proliferation (p < 0.05 or p < 0.01), migration (p < 0.05), and promoted cell apoptosis (p < 0.001) compared with the NC group. Down-regulated miR-16 exerted an opposite effect on primary human dermal fibroblasts with heat-denaturation. Furthermore, effects of miR16 down-regulation on cell proliferation and migration were reversed by HSP70 silence. CONCLUSION: MiR-16 might have an inhibitory effect on cell proliferation and migration in heat-denatured human dermal fibroblasts, and HSP70 might be associated with the cell proliferation and migration as a target gene of miR-16.

Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5

Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.

MicroRNA-221 promotes cell proliferation, migration, and differentiation by regulation of ZFPM2 in osteoblasts.

Bone fracture is a common medical condition, which may occur due to traumatic injury or disease-related conditions. Evidence suggests that microRNAs (miRNAs) can regulate osteoblast differentiation and function. In this study, we explored the effects and mechanism of miR-221 on the growth and migration of osteoblasts using MC3T3-E1 cells. The expression levels of miR-221 in the different groups were measured by qRT-PCR. Then, miR-221 mimic and inhibitor were transfected into MC3T3-E1 cells, and cell viability and migration were measured using the CCK-8 assay and the Transwell migration assay. Additionally, the expression levels of differentiation-related factors (Runx2 and Ocn) and ZFPM2 were measured by qRT-PCR. Western blot was used to measure the expression of cell cycle-related proteins, epithelial-mesenchymal transition (EMT)-related proteins, ZFPM2, and Wnt/Notch, and Smad signaling pathway proteins. miR-221 was significantly up-regulated in the patients with lumbar compression fracture (LCM) and trochanteric fracture (TF). miR-221 promoted ALP, Runx2, and OPN expressions in MC3T3-E1 cells. miR-221 overexpression significantly increased cell proliferation, migration, differentiation, and matrix mineralization, whereas suppression of miR-221 reversed these effects. Additionally, the results displayed that ZFPM2 was a direct target gene of miR-221, and overexpression of ZFPM2 reversed the promoting effects of miR-221 overexpression on osteoblasts. Mechanistic study revealed that overexpression of miR-221 inactivated the Wnt/Notch and Smad signaling pathways by regulating ZFPM2 expression. We drew the conclusions that miR-221 overexpression promoted osteoblast proliferation, migration, and differentiation by regulation of ZFPM2 expression and deactivating the Wnt/Notch and Smad signaling pathways.

Curcumin inhibits proliferation and enhances apoptosis in A549 cells by downregulating lncRNA UCA1.

OBJECTIVE: Curcumin has been reported to possess anti-tumor effects on multiple cancers, including lung cancer. However, the mechanisms of its anti-tumor effect on lung cancer have not been fully elucidated. Our study attempted to identify the effect of curcumin on A549 cells and further explore the potential mechanism. METHODS: Different concentrations of curcumin were exposed to A549 cells for 24 h and cell viability was measured by CCK-8 assay. The expression of UCA1 was overexpressed in A549 cells by transfection with pEX-UCA1. Cell proliferation was determined by BrdU staining and assessing the expression of CyclinD1 using western blot and RT-PCR assay. Apoptotic cells were measured by flow cytometry assay. Western blot was performed to assess the expression of apoptosis-related, Wnt and mTOR pathways-related factors. RESULTS: Curcumin incubation dramatically reduced viability of A549 cells in a dosage-dependent manner. Curcumin (0.6 µM) significantly reduced BrdU+-positive cells, declined the expression of CyclinD1, and enhanced cell apoptosis. Interestingly, we found that curcumin inhibited the expression of UCA1 and UCA1 overexpression abolished the effect of curcumin on cell apoptosis. In addition, we also found that curcumin inhibited Wnt and mTOR pathways through down-regulation of UCA1. CONCLUSION: We demonstrated that curcumin inhibited the growth of A549 cells through downregulation of UCA1, which might provide new insight for the treatment of lung cancer.

[ARTICLE WITHDRAWN] Long Noncoding RNA TUNAR Represses Growth, Migration, and Invasion of Human Glioma Cells Through Regulating miR-200a and Rac1.

THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHERS IN NOVEMBER 2020.

[ARTICLE WITHDRAWN] Knockdown of Long Noncoding RNA LINC00152 Suppresses Cellular Proliferation and Invasion in Glioma Cells by Regulating miR-4775.

THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHERS IN OCTOBER 2020.

Catechin protects rat cardiomyocytes from hypoxia-induced injury by regulating microRNA-92a.

Background: Myocardial infarction (MI) is a serious condition, caused by acute, persistent ischemia or hypoxia of a coronary artery and responsible for heart failure and sudden death. This study aimed to investigate the effects of catechin, one of the main active components of green tea, on hypoxia-induced MI cell model, as well as the underlying possible mechanism. Methods: Cell viability, proliferation, apoptosis, and the expression of microRNA-92a (miR-92a) after hypoxia stimulation and/or catechin treatment were assessed using cell counting kit-8 (CCK-8) assay, western blotting, annexin V-FITC/PI staining and qRT-PCR, respectively. miRNA transfection was performed to change the expression of miR-92a. The effects of miR-92a on hypoxia and catechin-treated H9c2 cell viability, proliferation and apoptosis were evaluated. Finally, western blotting was conducted to measure the expression of core factors in the c-Jun N-terminal kinase (JNK) signaling pathway. Results: Hypoxia stimulation significantly inhibited H9c2 cell viability and proliferation, induced cell apoptosis and up-regulated miR-92a expression. Catechin markedly protected H9c2 cells from hypoxia-induced viability loss, proliferation inhibition, and apoptosis enhance, as well as miR-92a expression increase. Furthermore, suppression of miR-92a enhanced the protective effects of catechin on hypoxia-induced H9c2 cells. Overexpression of miR-92a had opposite effects. Catechin activated the JNK pathway in H9c2 cells by down-regulating miR-92a. Conclusion: Catechin protected H9c2 cells from hypoxia-induced injury by regulating miR-92a and JNK signaling pathway. Our findings facilitate the understanding of the protective activity of catechin in hypoxia-induced MI cell injury and provide a theoretical basis for further explore treatment of MI by using catechin.

Lentinan up-regulates microRNA-340 to promote apoptosis and autophagy of human osteosarcoma cells.

BACKGROUND: Osteosarcoma (OS) is a common tumor of bone, and the high incidence and poor prognosis of OS call for novel therapeutic strategies. We aimed to explore the functional role of lentinan (LNT) in human OS MG63 cells as well as the underlying mechanisms. METHODS: Cell viability of MG63 cells under LNT stimulation was measured by CCK-8 assay to explore the adequate concentration of LNT. Cell proliferation, apoptosis and expression of microRNA (miR)-340 in MG63 cells after LNT treatments were assayed by BrdU incorporation assay, flow cytometry assay and quantitative reverse transcription PCR, respectively. Expression of proteins associated with cell cycle, apoptosis, and autophagy were determined by western blot analysis. Subsequently, whether LNT affected MG63 cells through miR-340 as well as the related signaling pathway was explored. RESULTS: Cell viability was reduced by 5-100 mg/mL of LNT. Percentage of BrdU-positive cells was reduced while that of apoptotic cells was enhanced by LNT treatment. LNT decreased cyclin D1 level but increased levels of active caspase-3 and caspase-9. After treatment, LNT enhanced LC3B-II/LC3B-I and Beclin-1 levels but reduced the p62 level. The miR-340 level was up-regulated by LNT, and further experiments showed LNT promoted apoptosis and autophagy through up-regulating miR-340. Moreover, LNT reduced the phosphorylated levels of MAPK and ERK through up-regulating miR-340. CONCLUSION: LNT reduced proliferation and induced apoptosis and autophagy by up-regulating miR-340 in MG63 cells, along with inhibition of the MAPK/ERK pathway.

MicroRNA-221 promotes cell proliferation, migration, and differentiation by regulation of ZFPM2 in osteoblasts

Bone fracture is a common medical condition, which may occur due to traumatic injury or disease-related conditions. Evidence suggests that microRNAs (miRNAs) can regulate osteoblast differentiation and function. In this study, we explored the effects and mechanism of miR-221 on the growth and migration of osteoblasts using MC3T3-E1 cells. The expression levels of miR-221 in the different groups were measured by qRT-PCR. Then, miR-221 mimic and inhibitor were transfected into MC3T3-E1 cells, and cell viability and migration were measured using the CCK-8 assay and the Transwell migration assay. Additionally, the expression levels of differentiation-related factors (Runx2 and Ocn) and ZFPM2 were measured by qRT-PCR. Western blot was used to measure the expression of cell cycle-related proteins, epithelial-mesenchymal transition (EMT)-related proteins, ZFPM2, and Wnt/Notch, and Smad signaling pathway proteins. miR-221 was significantly up-regulated in the patients with lumbar compression fracture (LCM) and trochanteric fracture (TF). miR-221 promoted ALP, Runx2, and OPN expressions in MC3T3-E1 cells. miR-221 overexpression significantly increased cell proliferation, migration, differentiation, and matrix mineralization, whereas suppression of miR-221 reversed these effects. Additionally, the results displayed that ZFPM2 was a direct target gene of miR-221, and overexpression of ZFPM2 reversed the promoting effects of miR-221 overexpression on osteoblasts. Mechanistic study revealed that overexpression of miR-221 inactivated the Wnt/Notch and Smad signaling pathways by regulating ZFPM2 expression. We drew the conclusions that miR-221 overexpression promoted osteoblast proliferation, migration, and differentiation by regulation of ZFPM2 expression and deactivating the Wnt/Notch and Smad signaling pathways.

MicroRNA­21 increases cell viability and suppresses cellular apoptosis in non­small cell lung cancer by regulating the PI3K/Akt signaling pathway.

MicroRNA (miRNA/miR), a type of non­coding RNA molecule, is able to inhibit the expression of target genes at multiple stagess. There are 800­1,000 known miRNAs in the human genome, which serve important roles in cell proliferation, differentiation, apoptosis and migration. Previous studies have demonstrated that the expression of miR­21 is upregulated in numerous types of malignant tumor, and that miR­21 participates in the occurrence and development of tumors via complex regulatory mechanisms. The present study aimed to investigate the association between miR­21 expression, cell viability and apoptosis in a lung cancer cell line, and to elucidate the potential mechanisms. miR­21 or small interfering RNA against miR­21 were transfected into A549 non­small cell lung cancer cells. The mRNA expression of miR­21 was confirmed. Cell viability and apoptosis were examined using MTT and flow cytometric assays, respectively. The expression of certain apoptosis­associated proteins was detected by western blotting. The results of the present study demonstrated that miR­21 was able to increase the proliferation of A549 cells by inhibiting cellular apoptosis. miR­21 inhibited apoptosis by modulating the activation of the phosphatidylinositol 3­kinase/Rac­α serine/threonine protein kinase (Akt) pathway in A549 cells. Correspondingly, inhibition of Akt decreased the apoptosis of A549 cells in miR­21 siRNA­treated cells. Therefore, the results of the present study demonstrated that miR­21 increased cell viability by inhibiting apoptosis, through regulation of Akt activation. The present study demonstrated that miR­21 may be involved in the progression of lung cancer and may be a novel therapeutic target for the disease.

Sox9 Protects against Human Lung Fibroblast Cell Apoptosis Induced by LPS through Activation of the AKT/GSK3ß Pathway.

Sex-determining region Y-box 9 (Sox9) is an important transcription factor that has been identified as a key regulator of several types of diseases. In this study, we explored the correlation of Sox9 with cell proliferation, apoptosis, inflammatory factor expression, and the possible signaling pathway in human lung fibroblast cell line to investigate the possible mechanism of neonatal pneumonia. Therefore, in the present study, pc-Sox9 and si-Sox9 were transfected into MRC-5 (human fetal lung fibroblast cell line) to promote or inhibit expression of Sox-9. Quantitative reverse-transcription polymerase chain reaction and Western blot were used to determine the expression level of Sox-9 at mRNA and protein level. Then 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry were used to explore, respectively, proliferation and apoptosis in vitro. We found that Sox9 could significantly upregulate the proliferation rate and inhibit apoptosis rate and inflammatory factor expression of MRC-5 cells compared with a control group. Moreover, the signaling pathway study confirmed that Sox9 protected MRC-5 from lipopolysaccharide injury through the AKT/GSK3ß pathway. All these findings suggest that Sox9 acts as a novel marker for neonatal pneumonia and could be a new therapeutic target for this disease.

Regulation function of MMP-1 downregulated by siRNA on migration of heat-denatured dermal fibroblasts.

Cutaneous wound healing is a complex physiological process that requires the efforts of various cell types and signaling pathways and often results in thickened collagen-enriched healed tissue called a scar. Therefore, the identification of the mechanism of cutaneous wound healing is necessary and has great value in providing better treatment. Here, we demonstrated that MMP-1 inhibition could promote cell proliferation in dermal fibroblasts via the MTT assay. Meanwhile, we investigated cell migration by flow cytometry and tested type I collagenase activity. We found that MMP-1 inhibition promoted cell proliferation and inhibited cell migration and type I collagenase activity. In conclusion, our study demonstrated that MMP-1 might be a potential therapeutic target in cutaneous wound healing.

MicroRNA-137 promotes hepatitis B virus gene expression and replication via targeting the protein inhibitor of activated STAT 2.

Hepatitis B virus (HBV) infection is one of the most important infectious diseases in China. In this study, we investigated the functional role of miR-137 in HBV infection to further elucidate the mechanism underlying the associated pathology. Viral replication was determined after transfection of HEK293 cells with the replication-competent vector pHBV1.3 and miR137 mimics or inhibitors. Expression of HBV genes was determined by quantitative real-time PCR (qRT-PCR). Expression of miR-137 and protein inhibitor of activated STAT 2 (PIAS2) was determined by qRT-PCR and Western blotting. Activity of the PIAS2 3'-UTR was determined by dual-luciferase reporter assays. Transfection of HEK293 cells with pHBV1.3 increased the expression of miR-137. Co-transfection with miR-137 mimic upregulated HBV gene expression and viral replication. MiR-137 targeted the PIAS2 3'-UTR, and suppressed PIAS2 mRNA and protein expressions. SiRNA-mediated PIAS2 knockdown suppressed HBV gene expression and viral replication. PIAS2 expression rescued the promotion effect of miR-137 on HBV expression and viral replication. MiR-137 expression was significantly upregulated following HBV infection. Furthermore, miR-137 promoted the expression of HBV genes and viral replication by targeting the expression of PIAS2. Our findings might provide a new insight into the diagnosis and treatment of HBV infection.