Preparation of Surface-Wrinkled Silica-Polystyrene Colloidal Composite Particles.

In this work, we report a facile emulsion swelling route to prepare surface-wrinkled silica-polystyrene (SiO2-PS) composite particles. Submicrometer-sized, near-spherical SiO2-PS composite particles were first synthesized by dispersion polymerization of styrene in an ethanol/water mixture, and then, surface-wrinkled SiO2-PS particles were obtained by swelling the SiO2-PS particles with a toluene/water emulsion and subsequent drying. It is emphasized that no surface pretreatment on the SiO2-PS composite particles is required for the formation of the wrinkled surface, and the most striking feature is that the surface-wrinkled particle was not deformed from a single near-spherical SiO2-PS composite particle but from many ones. The influence of various swelling parameters including toluene/particle mass ratio, surfactant concentration, stirring rate, swelling temperature, swelling time, and silica size on the morphology of the composite particles was studied. This method represents a new paradigm for the preparation of concave polymer colloids.

Creating High Regioselectivity by Electronic Metal-Support Interaction of a Single-Atomic-Site Catalyst.

Ligands are the most commonly used means to control the regioselectivity of organic reactions. It is very important to develop new regioselective control methods for organic synthesis. In this study, we designed and synthesized a single-atomic-site catalyst (SAC), namely, Cu1-TiC, with strong electronic metal-support interaction (EMSI) effects by studying various reaction mechanisms. π cloud back-donation to the alkyne on the metal catalytic intermediate was enhanced during the reaction by using transient electron-rich characteristics. In this way, the reaction achieved highly linear-E-type regioselective conversion of electronically unbiased alkynes and completely avoided the formation of branched isomers (ln:br >100:1, TON up to 612, 3 times higher than previously recorded). The structural elements of the SACs were designed following the requirements of the synthesis mechanism. Every element in the catalyst played an important role in the synthesis mechanism. This demonstrated that the EMSI, which is normally thought to be responsible for the improvement in catalytic efficiency and durability in heterogeneous catalysis, now first shows exciting potential for regulating the regioselectivity in homogeneous catalysis.

LncRNA PLAC 2 downregulated miR-21 in non-small cell lung cancer and predicted survival.

BACKGROUND: LncRNA PLAC2 has been characterized as a tumor suppressive lncRNA in glioma. We investigated the role of PLAC2 in non-small cell lung cancer (NSCLC). METHODS: A total of 187 NSCLC patients were admitted by The First Hospital of Jilin University from December 2010 to December 2014. All the patients were diagnosed by histopathological approaches. Transient cell transfections, RT-qPCR, invasion, and migration ability measurement, were applied for the experiments. RESULTS: PLAC2 was down-regulated, while miR-21 was up-regulated in NSCLC tissues compared to non-cancer tissues. Low PLAC2 levels in NSCLC tissues were associated with poor survival of NSCLC patients. PLAC2 and miR-21 were inversely correlated, and PLAC 2 over-expression in NSCLC cells resulted in the down-regulation of miR-21. However, miR-21 over-expression did not significantly affect PLAC2 expression. In addition, PLAC2 over-expression resulted in decreased migration and invasion rates of NSCLC cells. MiR-21 over-expression played the opposite role and attenuated the effects of PLAC2 over-expression. CONCLUSIONS: In conclusion, lncRNA PLAC2 down-regulated miR-21 in NSCLC and inhibited cancer cell migration and invasion.

Inhibition of C-X-C Motif Chemokine 10 (CXCL10) Protects Mice from Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease.

BACKGROUND Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow. COPD can progress to persistent decline of pulmonary function. This study explored the effect of CXCL10 on COPD induced by cigarette smoke (CS) and its underlying mechanism. MATERIAL AND METHODS Wild-type (WT) mice were randomly assigned into 3 groups: the control group, the CS group, and the intervention group. Mice in the CS group were exposed to CS and mice in the CXCL10 group were exposed to CS and CXCL10 neutralizing antibody. At 24 h after the last CS exposure, body weight and lung functions of each mouse were recorded. Mice were then anesthetized for collecting bronchoalveolar lavage fluid (BALF) and lung tissues. Levels of interleukin-6 (IL-6), keratinocyte chemotactic factor (KC), and monocyte chemoattractant protein-1 (MCP-1) in supernatant and lung homogenate were detected by ELISA and real-time PCR (RT-PCR), respectively. For in vitro experiments, human bronchial epithelial cells 16HBE were stimulated with different concentrations of cigarette smoke extract (CSE) and CXCL10. Cell viability and levels of inflammatory cytokines in the cell supernatant were detected by Cell Counting Kit-8 (CCK-8) and ELISA assay, respectively. RESULTS Our data showed significant weight loss and reduction of lung functions in mice in the CS group compared with those in the control group and intervention group. Increased levels of IL-6, KC, and MCP-1 in BALF and lung homogenate were observed in mice in the model group compared to those in the control group and intervention group. In vitro experiments also confirmed that CXCL10-neutralizing antibody can inhibit CSE-induced cell necrosis and activation of inflammatory cytokines. CONCLUSIONS Inhibited CXCL10 protects against COPD progression by decreasing secretion of inflammatory factors, which provides a new direction for the clinical prevention and treatment of COPD.

A Novel Long Noncoding RNA (lncRNA), LL22NC03-N64E9.1, Promotes the Proliferation of Lung Cancer Cells and is a Potential Prognostic Molecular Biomarker for Lung Cancer.

BACKGROUND The aim of this study was to investigate the expression of a novel long noncoding RNA (lncRNA), LL22NC03-N64E9.1, and its effect on the phenotype of lung cancer cells and tissues using The Cancer Genome Atlas (TCGA) RNA sequencing data and other publicly available profiling data. MATERIAL AND METHODS The lung cancer dataset GSE30219 was downloaded from the Gene Expression Omnibus (GEO) repository. Differentially expressed lncRNA, LL22NC03-N64E9.1, in 48 lung cancer tissue samples and adjacent normal lung tissues, normal lung cell lines BEAS-2B and A549, and lung cancer cell lines, H1703, and H292, were detected by quantitative reverse transcription polymerase chain reaction (PCR) (qRT-PCR). Interference efficiency was performed using small interfering RNA (siRNA). Tumor levels of lncRNA, LL22NC03-N64E9.1, and clinicopathological parameters were statistically analyzed. RESULTS Analysis of the GSE30219 test cohort showed that lncRNA, LL22NC03-N64E9.1 expression was significantly increased in lung cancer. In clinical tissue samples, the level of LL22NC03-N64E9.1 in patients with lung cancer was significantly increased compared with adjacent normal lung tissues (P<0.001). The level of LL22NC03-N64E9.1 in patients with lung cancer was significantly correlated with tumor size and TNM stage (P<0.05), but not with age, sex and the presence of lymph node metastasis (P>0.05). In the H292 cells, following knockdown of LL22NC03-N64E9.1, cell proliferation and cloning were reduced. CONCLUSIONS Expression of lncRNA, LL22NC03-N64E9.1, promoted proliferation of lung cancer cells in vitro, was highly expressed in lung cancer tissues and was associated with increased overall survival (OS), tumor size, and tumor stage in patients with lung cancer.

Erratum to: Suppression of Spry4 enhances cancer stem cell properties of human MDA-MB-231 breast carcinoma cells.

[This corrects the article DOI: 10.1186/s12935-016-0292-7.].

Suppression of Spry4 enhances cancer stem cell properties of human MDA-MB-231 breast carcinoma cells.

BACKGROUND: Cancer stem cells contribute to tumor initiation, heterogeneity, and recurrence, and are critical targets in cancer therapy. Sprouty4 (Spry4) is a potent inhibitor of signal transduction pathways elicited by receptor tyrosine kinases, and has roles in regulating cell proliferation, migration and differentiation. Spry4 has been implicated as a tumor suppressor and in modulating embryonic stem cells. OBJECTIVES: The purpose of this research was to test the novel idea that Spry4 regulates cancer stem cell properties in breast cancer. METHODS: Loss-of function of Spry4 in human MDA-MB-231 cell was used to test our hypothesis. Spry4 knockdown or control cell lines were generated using lentiviral delivery of human Spry4 or non-targeting control shRNAs, and then selected with 2 µg/ml puromycin. Cell growth and migratory abilities were determined using growth curve and cell cycle flow cytometry analyses and scratch assays, respectively. Xenograft tumor model was used to determine the tumorigenic activity and metastasis in vivo. Cancer stem cell related markers were evaluated using immunoblotting assays and fluorescence-activated cell sorting. Cancer stem cell phenotype was evaluated using in vitro mammosphere formation and drug sensitivity tests, and in vivo limiting dilution tumor formation assay. RESULTS: Two out of three tested human Spry4 shRNAs significantly suppressed the expression of endogenous Spry4 in MDA-MB-231 cells. Suppressing Spry4 expression increased MDA-MB-231 cell proliferation and migration. Suppressing Spry4 increased ß3-integrin expression, and CD133(+)CD44(+) subpopulation. Suppressing Spry4 increased mammosphere formation, while decreasing the sensitivity of MDA-MB-231 cells to Paclitaxel treatment. Finally, suppressing Spry4 increased the potency of MDA-MB-231 cell tumor initiation, a feature attributed to cancer stem cells. CONCLUSIONS: Our findings provide novel evidence that endogenous Spry4 may have tumor suppressive activity in breast cancer by suppressing cancer stem cell properties in addition to negative effects on tumor cell proliferation and migration.

Coordination polymer submicrospheres: fast microwave synthesis and their conversion under different atmospheres.

Rare earth (RE) based coordination polymer (CP) submicrospheres have been prepared from pyridine-2,5-dicarboxylic acid and RE(NO3)3 via a facile microwave heating method in 5 min, with N,N-dimethylformamide (DMF) as solvent. The submicrospheres have diameters of 100-400 nm. Furthermore, the surface of the microspheres is smooth and the microspheres are solid. Several CP submicrospheres (RE = La, Gd, Y) were selected and calcined under different atmospheres (including air, N2, and NH3). After calcination in air at 550 °C for 4 h, rare earth oxide (RE2O3) submicrospheres were obtained. On calcination under an N2 atmosphere, LaN/La2O3/C composite spheres were obtained for La-based CPs. For Gd(Y)-based CPs, Gd2O3(Y2O3)/C composite spheres were obtained. Porous carbon submicrospheres were obtained after the removal of RE2O3 and REN from the composite spheres. Interestingly, under an NH3 atmosphere, La2O2CN2 submicrospheres were produced from the La-based CPs. In addition, the Gd-based and Y-based CPs submicrospheres gave Gd2O3/GdN/C and Y2O3/C submicrospheres, respectively. As examples of their potential applications, their upconversion properties and electrochemical properties of the as-prepared products were investigated. This facile microwave synthesis method may offer an attractive approach for the preparation of other RE-CP micro-/nanostructures, and many interesting materials may be derived.

Efficient Electrochemical Reduction of CO2 on g-C3 N4 Monolayer-supported Metal Trimer Catalysts: A DFT Study.

The electrochemical reduction of CO2 into valuable chemicals and fuels is a promising but challenging method to realize the carbon cycle. In this work, a series of transition metal trimer clusters supported on g-C3 N4 catalysts (M3 @g-C3 N4 , M=Cr, Mn, Fe, Co, Ni, Cu, and Ru) for electrochemical CO2 reduction (CO2 RR) toward C1 and C2 products were systemically studied using density functional theory (DFT) calculations. Our results show that CO2 could be adsorbed and activated effectively on M3 @g-C3 N4 from adsorption configurations and electronic structures analyses. Cu3 @g-C3 N4 is a promising electrocatalyst for CH4 production with a limiting potential of -0.42 V. Cr3 @g-C3 N4 , Fe3 @g-C3 N4 , and Co3 @g-C3 N4 produce a low limiting potential of -0.64 V, -0.45 V, and -0.64 V for C2 H4 production, respectively. Hydrogen evolution reaction is refrained on Cu3 @g-C3 N4 , Cr3 @g-C3 N4 , and Co3 @ g-C3 N4 . This work provides useful insights into transition metal trimer cluster catalysts with enhanced activity and selectivity in CO2 RR.

Single-atom-catalyst with abundant Co-S4 sites for use as a counter electrode in photovoltaics.

Herein, a 7.35 wt% Co loading C-SAC is synthesized by pyrolysis of Co-MOF-74 in a strongly polar molten salt system. In dye-sensitized solar cells, this SAC based counter electrode shows higher photoelectric conversion efficiency than the Pt counter electrode. This work provides new insights for the preparation and application of C-SACs.

Salt melt synthesis of Chlorella-derived nitrogen-doped porous carbon with atomically dispersed CoN4 sites for efficient oxygen reduction reaction.

Carbon-supported single-atom catalysts (C-SACs) demonstrate great potential in various key electrochemical reactions. Nevertheless, the development of facile and economical strategies is highly appealing yet challenging given that the commonly used pyrolysis method has strict requirements on the structure and composition of precursors. Here, we demonstrate for the first time a facile and low-cost pyrolysis strategy assisted by molten salts at high temperature for preparing porous C-SACs with well-dispersed Co-N4 sites directly from a Chlorella precursor. Based on the X-ray absorption fine structure results and aberration-corrected scanning transmission electron microscopy images, we show that single atom Co-N4 moieties are anchored on a carbon matrix. A porous structure with a large specific surface area (2907 m2 g-1) and atomically dispersed active sites of Co provide the as-prepared Co-N/C-SAC with excellent electrocatalytic activity and stability for the ORR. The electrochemical measurements show that the half-wave potential and limited current density of this material are 0.83 V vs. RHE and 5.5 mA cm-2, respectively, which are comparable to those of commercial Pt/C.

Molecular mechanism of AQP3 in regulating differentiation and apoptosis of lung cancer stem cells through Wnt/GSK-3ß/ß-Catenin pathway.

PURPOSE: The refractory nature and proneness to recurrence of lung cancer are related to the proliferation and differentiation of lung cancer stem cells (LCSCs). This paper aims to explore the effect of aquaporin-3 (AQP3) on the functions of LCSCs, and its molecular mechanism in regulating the differentiation and apoptosis of LCSCs through the Wnt/glycogen synthase kinase-3ß (GSK-3ß)/ß-catenin pathway. METHODS: The stem cells were selected and the cell lines with low expression of AQP3 were constructed, followed by transcriptome sequencing. LCSCs were transfected with empty lentivirus in the control group and transfected with AQP3 shRNA in the interference group, and the low expression of AQP3 was inhibited using the Wnt pathway inhibitor XAV939 in the interference+inhibitor group. The expressions of AQP3, Wnt/GSK-3ß/ß-catenin pathway genes, stemness genes, differentiation-related markers and apoptosis proteins in LCSCs were detected. RESULTS: In the interference group, the pathway genes were highly expressed. The genes in the interference group were enriched in the Wnt/GSK-3ß/ß-catenin pathway. In the interference group, the expressions of ß-catenin, GSK-3ß and signal transducer and activator of transcription 3 (STAT3) were significantly higher, while the expression of adenomatous polyposis coli (APC) was significantly lower (p<0.05). The expression of Wnt5α had no difference. In the interference group, the expressions of stemness-related genes were obviously higher, while the expression of CDK2 had no difference (p=0.471). The interference group had higher expressions of differentiation markers. CONCLUSION: AQP3 can reduce the differentiation and inhibit the apoptosis of LCSCs through reducing the expressions of Wnt/GSK-3ß/ß-catenin pathway-related genes such as ß-catenin, GSK-3ß and STAT3, thereby affecting the tumor progression.

Molecular mechanism of aquapontin (AQP3) in regulating differentiation and apoptosis of lung cancer stem cells through Wnt/GSK-3ß/ß-Catenin pathway.

PURPOSE: To explore the effect of aquaporin-3 (AQP3) on the functions of lung cancer stem cells (LCSCs), and its molecular mechanism in regulating the differentiation and apoptosis of LCSCs through the Wnt/glycogen synthase kinase-3ß (GSK-3ß)/ß-catenin pathway. METHODS: The stem cells were selected and the cell lines with low expression of AQP3 were constructed, followed by transcriptome sequencing. LCSCs were transfected with empty lentivirus in control group and transfected with AQP3 shRNA in interference group, and the low expression of AQP3 was inhibited using the Wnt pathway inhibitor XAV939 in interference + inhibitor group. The expressions of AQP3, Wnt/GSK-3ß/ß-catenin pathway genes, stemness genes, differentiation-related markers and apoptosis proteins in LCSCs were detected. RESULTS: In interference group, the pathway genes were highly expressed. The genes in interference group were enriched in the Wnt/GSK-3ß/ß-catenin pathway. In interference group, the expressions of ß-catenin, GSK-3ß and signal transducer and activator of transcription 3 (STAT3) were significantly higher, while the expression of adenomatous polyposis coli (APC) was significantly lower (p<0.05). The expression of Wnt5α had no difference. In interference group, the expressions of stemness-related genes were obviously higher, while the expression of CDK2 had no difference (p=0.471). Interference group had higher expressions of differentiation markers. CONCLUSION: In conclusion, AQP3 can reduce the differentiation and inhibit the apoptosis of LCSCs through reducing the expressions of Wnt/GSK-3ß/ß-catenin pathway-related genes such as ß-catenin, GSK-3ß and STAT3, thereby affecting the tumor progression.

L-cysteine functionalized straticulate C3N4 for the selective enrichment of glycopeptides.

The facile enrichment of glycopeptides or glycoproteins poses great challenges for glycoproteomic research. In this study, a novel hydrophilic material, named zwitterionic hydrophilic L-cysteine derivatized straticulate-C3N4 composites (LCAC), were synthesized and evaluated for the enrichment of N-glycopeptides. LCAC exhibited good biocompatibility, excellent hydrophilicity and selectivity, by virtue of the large surface of C3N4 and the zwitterionic property offered by cysteine. LCAC demonstrated excellent performance for N-glycopeptide enrichment with the sensitivity of 0.033 fmol/µL, selectivity of 1:100, and high recovery rate (∼85%). The performance of LCAC was demonstrated by the identification of 35 N-glycopeptides from IgG, as well as capturing 1809 human urine N-glycopeptides corresponding to 876 N-glycoproteins. Comparing the LCAC with our developed phenylboronic acid functionalized material showed a certain complementary due to the different binding mechanism. The simple production and enhanced hydrophilic properties make the material a promising choice for glycoproteomics researches.

MicroRNA-141-3p affected proliferation, chemosensitivity, migration and invasion of colorectal cancer cells by targeting EGFR.

Colorectal cancer (CRC) is one of the most often diagnosed cancers globally. MicroRNAs are small RNA molecules that play essential roles in tumorigenesis and progression of CRC. Here we evaluated the effects of miR-141-3p on growth, cetuximab sensitivity, migration and invasion of CRC cells. We found that miR-141-3p negatively regulated the proliferation, migration and invasion in CRC cells. In addition, miR-141-3p enhanced the cetuximab sensitivity of CRC cells by EGFR suppression. Moreover, miR-141-3p improved cetuximab-induced apoptosis in CRC cells. Furthermore, miR-141-3p altered the expression of E-cadherin, N-cadherin, snail and Vimentin, indicating miR-141-3p might play a role on epithelial to mesenchymal transition (EMT). Luciferase reporter assay showed that EGFR was the direct binding site of miR-141-3p and the expression levels of p-EGFR, Raf-1, pAKT and p-ERK1/2 were regulated by miR-141-3p. After down-regulation of EGFR by siRNA in CRC cells, the effects of miR-141-3p on proliferation, migration and invasion were reversed. miR-141-3p played important roles in CRC growth and response to cetuximab treatment, and might function as a potential biomarker to predict cetuximab response.

[Corrigendum] Butein induces cell apoptosis and inhibition of cyclooxygenase­2 expression in A549 lung cancer cells.

Following the publication of the above article, the authors have realized that an error was made in the Acknowledgements section in this paper; this research was not, in fact, supported by a grant from the National Natural Science Foundation of Jilin (Project no. 83657488), as had been stated. The authors regret their oversight in providing this incorrect information in the Acknowledgements section of their paper. They thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Molecular Medicine Reports 9: 763-767, 2014; DOI: 10.3892/mmr.2013.1850].

[Retracted] Downregulation of NOB1 suppresses the proliferation and tumor growth of non­small cell lung cancer in vitro and in vivo.

Oncol Rep 31: [Related article:] 1271­1276, 2014; DOI: 10.3892/or.2014.2991. The authors wish to retract their article entitled 'Down-regulation of NOB1 suppresses the proliferation and tumor growth of non­small cell lung cancer in vitro and in vivo', published in Oncology Reports 31: 1271­1276, 2014. The authors have identified that the results shown in Fig. 4A did not display a significant level of difference comparing among the groups, which undermines the conclusions stated in the article. In addition, the 'Acknowledgements' section featured an error in terms of the quoted project number. For these reasons, the authors have decided to withdraw this paper from the Journal. All the named authors agree to this retraction. and regret any inconvenience to the readers and to the Editor of Oncology Reports that this retraction will cause.

Upregulation of E-cadherin in bronchoalveolar lavage fluid-derived exosomes in patients with lung cancer.

BACKGROUND: Lung cancer features extremely high rates of morbidity and mortality. Bronchoalveolar lavage fluid (BALF), obtained by bronchoscopy and bronchoalveolar perfusion, can provide information on the cellular components of the lung microenvironment to assist with diagnosis and treatment of lung cancer. METHODS: BALF was performed using a flexible bronchofiberscope. Exosomes were collected by ultracentrifugation. ELISA detected the amount of E-cadherin. Transmission electron microscopic, ELISA and WB were conducted to identify the existence of the exosomes. Transwell and Wound healing assays were used to detect the ability of migration and invasion. RESULTS: We identified the existence of exosomes in BALF. Furthermore, we observed larger amounts of E-cadherin in the BALF obtained from patients with lung cancer than in the control obtained from the healthy side of pneumonia. Exosomes from lung cancer groups promoted the migration and invasion of A549 cancer cells. CONCLUSION: The exosomes from lung cancer BALF promoted the migration and invasion of A549 cancer cells by carrying E-cadherin. E-cadherin on the surface of exosomes may act through a VE-cadherin dependent mechanism and induce lung cancer metastasis.

Long noncoding RNA CRNDE promotes non-small cell lung cancer progression via sponging microRNA-338-3p.

BACKGROUND: The long noncoding RNA colorectal neoplasia differentially expressed (CRNDE) was reported to be involved in the initiation and development of multiple cancers. However, the detailed biological role of CRNDE in non-small cell lung cancer (NSCLC) remains largely unclear. Herein, we aimed to explore the biological function and underlying molecular mechanism of CRNDE in NSCLC. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the expression of CRNDE in NSCLC tissues and cell lines. Cell counting kit-8 (CCK-8), colony formation, flow cytometry, wound-healing, and transwell invasion assays were applied to detect cell proliferation, colony formation, cycle arrest progression, migration and invasion, respectively. Novel targets of CRNDE were selected with bioinformatics software and were confirmed using luciferase reporter and RNA immunoprecipitation assays. To detect the role of CRNDE in vivo tumorigenesis, tumor xenografts were created. RESULTS: CRNDE expression is remarkably upregulated in NSCLC tissues and cell lines. Upregulated CRNDE expression was positively associated with advanced tumor-node-metastasis (TNM) stage, lymph node metastasis and poor overall survival of patients with NSCLC. Function assays demonstrated that knockdown of CRNDE significantly inhibited NSCLC cell proliferation, colony formation, migration and invasionin vitro, and decreased the xenograft tumor volume and weight in vitro. We uncovered that miR-338-3p is a downstream target of CRNDE and that miR-338-3p inhibition partially reversed the CRNDE depletion-mediated inhibitory effect on cell proliferation, colony formation, migration and invasion in NSCLC cells. CONCLUSION: These findings indicated that CRNDE functions as an oncogene that exerts important regulatory roles in NSCLC progression via sponging miR-338-3p.

Overexpression of the long non-coding RNA Oprm1 alleviates apoptosis from cerebral ischemia-reperfusion injury through the Oprm1/miR-155/GATA3 axis.

Numerous differentially expressed long non-coding RNAs (lncRNAs) have been identified in cerebral ischemia-reperfusion (I/R) injury using RNA-Seq analysis. However, little is known about whether and how lncRNAs are involved in cerebral I/R injury. In this study, we investigated the function of the lncRNA Oprm1 in cerebral I/R injury and explored the underlying mechanism. An oxygen-glucose deprivation model in N2a cells was utilized to mimic cerebral I/R injury in vitro. Trypan blue staining, terminal deoxytransferase-mediated dUTP-biotin nick end labelling and caspase-3 were measured to evaluate apoptosis. Middle cerebral artery occlusion was performed in mice to evaluate the function of lncRNA Oprm1 in vivo. Real-time PCR and western blotting were used to measure the expression levels of lncRNA Opmr1, caspase-3, miR-155, GATA binding protein 3 (GATA3) and nuclear factor (NF)-κB. lncRNA Oprm1 was mainly located in the cytoplasm. Overexpression of lncRNA Oprm1 alleviated the apoptosis induced by oxygen-glucose deprivation and significantly reduced cleaved caspase-3 levels. Infarct size was distinctly decreased in the lncRNA Oprm1-overexpression group. The neurological score was also improved. Our findings showed that the lncRNA Oprm1/miR-155/GATA3 axis plays an important role in cerebral I/R injury. lncRNA Oprm1 may attenuate cerebral injury through the NF-κB pathway. lncRNA Oprm1 may serve as a potential target for new therapeutic interventions in patients with ischemic stroke.