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.

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.

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.

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.

[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].

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.

[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.

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.

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.

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.

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.

Vitamin D3-vitamin D receptor axis suppresses pulmonary emphysema by maintaining alveolar macrophage homeostasis and function.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by emphysema and/or obstructive bronchiolitis. Deficiency in vitamin D3 (VD3), which regulates gene expression through binding to vitamin D receptor (VDR), is associated with high risks of COPD susceptibility. Alveolar macrophages (AM), which are generated during early ontogeny and maintained in alveoli by self-renewal in response to cytokine GM-CSF, are positively correlated with severity of emphysema. However, whether and how VD3, VDR and AM interact to contribute to COPD pathogenesis at the molecular and cellular levels are largely unknown. METHODS: We used systems biology approaches to analyze gene expression in mouse macrophages from different tissues to identify key transcription factors (TF) for AM and infer COPD disease genes. We used RNA-seq and ChIP-seq to identify genes that are regulated by VD3 in AM. We used VDR-deficient (Vdr-/-) mice to investigate the role of VD3-VDR axis in the pathogenesis of COPD and characterized the transcriptional and functional alterations of Vdr-/- AM. FINDINGS: We find that VDR is a key TF for AM and a COPD disease gene. VDR is highly expressed in AM and in response to VD3 inhibits GM-CSF-induced AM proliferation. In Vdr-/- AM, genes involved in proliferation and immune response are upregulated. Consistently, Vdr-/- mice progressively accumulate AM and concomitantly develop emphysema without apparent infiltration of immune cells into the lung tissue. Intratracheal transfer of Vdr-/- AM into wildtype mice readily induces emphysema. The production of reactive oxygen species at basal level and in response to heme or lipopolysaccharide is elevated in Vdr-/- AM and suppressed by VD3 in wildtype AM. INTERPRETATION: These results show that the VD3-VDR axis is critical to counteract GM-CSF-induced AM proliferation and defect in this regulation leads to altered AM homeostasis and function. Our findings identify that VD3 deficiency contributes to emphysema by altering AM function without contributing to bronchiolitis. Our findings also suggest possibilities of modulating the VD3-VDR axis for inhibiting emphysema in COPD patients.

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.

Phenylboronic acid functionalized C3N4 facultative hydrophilic materials for enhanced enrichment of glycopeptides.

It is challenging to capture N-glycopeptides with high recovery and high specificity from complicated biosystems. Herein, we present a facile and economical procedure to generate a novel self-assembling 4-Mercaptobenzene boronic acid functionalized and Au-doped Straticulate C3N4 (MASC), with enhanced affinity capability towards glycopeptides. The materials possess low pH value adaptation, high hydrophilicity and stability, good repeatability and recyclability, and provided high selectivity (1:100), low limit of detection (0.33 fmol/µL), high enrichment efficiency (~ 80%) and high recovery rate (~ 90%) towards glycopeptides. The materials can capture glycopeptides unbiasedly, as demonstrated by the identification of 37 glycopeptides from IgG and 21 glycopeptides from horseradish peroxidase (HRP). The performance of MASC on human urine and serum glycoproteome analysis was also tested. An average of 1465 glycopeptides from 839 glycoproteins and 1553 glycopeptides from 884 glycoproteins were identified from female and male urine samples in a single mass spectrometry analysis. O-glycopeptides from human urine were also significantly enriched. Additionally, 463 glycopeptides assigned to 209 glycoproteins were identified from 5 µL of human serum. All of these results indicate that MASC presents a good performance and applicability in the field of glycoproteomic research.

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.

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.

Long noncoding RNA HOXD-AS1 promotes non-small cell lung cancer migration and invasion through regulating miR-133b/MMP9 axis.

HOXD antisense growth associated long noncoding RNA (HOXD-AS1) was reported to be dysregulated and exert crucial roles in tumorigenesis and progression of multiple malignancies. However, the role and mechanism of action of HOXD-AS1 in the carcinogenesis and progression of non-small lung cell cancers (NSCLC) remains largely unknown. HOXD-AS1, miR-133a and Matrix metallopeptidase 9 (MMP-9) mRNA expression were detected by quantitative real-time polymerase chain reaction assays in NSCLC tissues and cell lines. Cell counting kit-8, wound healing and transwell invasion assays were performed to evaluate cell proliferation, migration and invasion abilities, respectively. Luciferase assays were used to investigate binding seeds between miR-133b and HOXD-AS1. Western blot assay were performed to detect protein expression. Here higher expression of HOXD-AS1 was found in NSCLC tumor tissues compared with normal lung tissues, and was associated with lymph node metastasis, high tumor node metastasis (TNM) stage, and poor overall survival rate of patients with NSCLC. Knockdown of HOXD-AS1 significantly inhibited proliferation, migration and invasion of NSCLC cells. Additionally, we found that miR-133b was a direct downstream target of HOXD-AS1 in NSCLC. miR-133b inhibition reverse the inhibitory effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of MMP-9 (a target of miR-133b) in NSCLC cells. These results suggest that HOXD-AS1 might be a potential prognostic biomarker and a novel therapeutic target for treating NSCLC.