miR-22-3p Suppresses Endothelial Progenitor Cell Proliferation and Migration via Inhibiting Onecut 1 (OC1)/Vascular Endothelial Growth Factor A (VEGFA) Signaling Pathway and Its Clinical Significance in Venous Thrombosis.

BACKGROUND Proliferation and migration play crucial roles in various physiological processes, especially in injured endothelial repair. Endothelial progenitor cells (EPCs), as the precursors of endothelial cell, are involved in the regeneration of the endothelial lining of blood vessels. Furthermore, EPCs were found to be a potential choice for venous thrombosis (VT) treatment. MATERIAL AND METHODS EPCs were isolated from human peripheral blood of healthy adults and VT patients. Differently expressed micro(mi)RNAs were examined by quantitative real-time polymerase chain reaction, after which proliferative capacity and migration effect were tested by Cell-Counting Kit 8, scratch wound assay, and transwell assays. Bioinformatic analysis was applied to investigate the potential target messenger ribonucleic acid and a dual-luciferase reporting system was utilized to confirm the binding of miR-22-3p to its target gene. Western blot was carried out to detect candidate protein expression level. Finally, miR-22-3p expression was monitored in VT patients during follow-up to assess its correlation with prognosis of VT. RESULTS Our data revealed that miR-22-3p was upregulated in EPCs derived from deep VT (DVT) individuals and suppression of miR-22-3p contributed to proliferation and migration of EPCs. In addition, miR-22-3p/onecut 1 (OC1)/vascular endothelial growth factor A (VEGFA) signaling pathway was involved in regulating EPC migration and proliferation. In addition, lower expression of miR-22-3p in DVT patients indicated decreased risk of VT recurrence. CONCLUSIONS Our results suggest that miR-22-3p regulates OC1/VEGFA signaling and is involved in regulating EPC proliferation and migration. The expression level of miR-22-3p could be monitored to predict DVT patients' prognosis.

Exercise and Asthma.

Asthma is a chronic lower respiratory disease that is very common worldwide, and its incidence is increasing year by year. Since the 1970s, asthma has become widespread, with approximately 300 million people affected worldwide and about 250,000 people have lost their lives. Asthma seriously affects people's physical and mental health, resulting in reduced learning efficiency, limited physical activities, and decreased quality of life. Therefore, raising awareness of the risk of asthma and how to effectively treat asthma have become important targets for the prevention and management of asthma in recent years. For patients with asthma, exercise training is a widely accepted adjunct to drug-based and non-pharmacological treatment. It has been recommended abroad that exercise prescriptions are an important part of asthma management.

Exercise and Cystic Fibrosis.

Cystic fibrosis (CF) is an autosomal recessive, inherited congenital disease caused by the mutation of the family autosomal CF gene, with cumulative exocrine secretion characterized by inflammation, tracheal remodeling, and mucus accumulation. With the development of modern medical technology, CF patients are living longer lives and receiving more and more treatments, including traditional drugs, physical therapy, and gene therapy. Exercise is widely used to prevent and treat metabolic diseases such as cardiovascular diseases, obesity, diabetes, and metabolic syndrome. Regular exercise is beneficial to aerobic capacity and lung health. Exercise therapy has been of great interest since people realized that CF can be affected by exercise. Exercise alone can be used as an ACT (airway clearance technique), which promotes the removal of mucosal cilia. Exercise therapy is more easily accepted by any society, which helps to normalize the lives of CF patients, rather than placing a psychological burden on them. In this chapter, we will review the latest research progress about exercise in CF.

High KIF2A expression promotes proliferation, migration and predicts poor prognosis in lung adenocarcinoma.

The Kinesin family member 2a (KIF2A), that belongs to the Kinesin-13 microtubule depolymerases, plays an important role in cancer cell proliferation, migration and apoptosis in various types of cancer such as gastric cancer, breast cancer, and squamous cell carcinoma of the oral tongue, but, its role and mechanism in lung adenocarcinoma (LUAD) is largely unknown. The present study reported that KIF2A was overexpressed in LUAD tissues as compared with adjacent normal tissues. KIF2A was closely correlated with TNM stage and lymph node metastasis (P < 0.01), whereas, no similar relationships between KIF2A and age, gender, smoking and differentiation. Multivariate analysis indicated that hyperexpression of KIF2A in LUAD was an independent risk factor for worse overall survival in LUAD patients (HR: 3.135, 95%CI: 1.331-7.112, p < 0.05). In vitro, KIF2A knockdown markedly reduced LUAD cell A549 migration and could regulate epithelial-mesenchymal transition. Furthermore, silencing KIF2A inhibited cell proliferation and induced apoptosis in lung adenocarcinoma(LUAD) cells. In conclusion, KIF2A may serve as a valuable prognostic indicator and promising therapeutic target of LUAD.

An Overview of Muscle Atrophy.

Muscle is the most abundant tissue in human body, and it can be atrophy when synthesis is inferior to degradation. Muscle atrophy is prevalent as it is a complication of many diseases. Besides its devastating effects on health, it also decreases life quality and increases mortality as well. This review provides an overview of muscle atrophy, including its prevalence, economic and health burden, and clinical therapy. Its clinical therapy includes exercise training, nutritional therapy, electrical stimulation, and drugs such as testosterone and ghrelin/IGF-1 analogues. More large-scale, long-term clinical trials are needed for therapies for muscle atrophy. In addition, more therapeutic targets are highly needed.

Circular RNAs in Vascular Functions and Diseases.

Vascular disease is one of the top five causes of death and affects a variety of other diseases, such as heart, nervous system, and metabolic disorders. Vascular dysfunction is a hallmark of ischemia, cancer, and inflammatory diseases and can accelerate the progression of diseases. Circular RNAs (circRNAs) are a new type of noncoding RNAs with covalent bond ring structure, which have been reported to be abnormally expressed in many human diseases. circRNAs regulate gene expression through the sponging of microRNAs (miRNAs) and can also be used as disease biomarkers. Here we will summarize the functions of circRNAs in vascular diseases, including vascular dysfunction, atherosclerosis, diabetes mellitus-related retinal vascular dysfunction, chronic thromboembolic pulmonary hypertension, carotid atherosclerotic disease, hepatic vascular invasion in hepatocellular carcinoma, aortic aneurysm, coronary artery disease, and type 2 diabetes mellitus.

C/EBPB-CITED4 in Exercised Heart.

C/EBPB is a crucial transcription factor, participating in a variety of biological processes including cell proliferation, differentiation and development. In the cardiovascular system, C/EBPB-CITED4 signaling is known as a signaling pathway mediating exercise-induced cardiac growth. After its exact role in exercised heart firstly reported in 2010, more and more evidence confirmed that. MicroRNA (e.g. miR-222) and many molecules (e.g. Alpha-lipoic acid) can regulate this pathway and then involve in the cardiac protection effect induced by endurance exercise training. In addition, in cardiac growth during pregnancy, C/EBPB is also a required regulator. This chapter will give an introduction of the C/EBPB-CITED4 signaling and the regulatory network based on this signaling pathway in exercised heart.

Cardioprotective Effects of Exosomes and Their Potential Therapeutic Use.

Exosomes are membrane-contained vesicles released by various types of cells both in animals and human. They contain microRNAs and proteins and can travel to target cells, affecting their functions. There are specific factors on the surface of every exosomes, making sure that they will be taken up by certain type of cells. With these features, exosomes have been recognized to be one of the fundamental "messengers" for cell-cell communication. Recently, increased interest has been raised in exosomes since they were discovered to play an unneglectable role in preserving cardiac function and cardiomyocyte repair during stress. The widely explored stem cell therapy for cardiomyopathy uncovered the contribution of exosomes. Here we summarized cardioprotective effects of exosomes and their potential therapeutic use.

Therapeutic Effects of Ischemic-Preconditioned Exosomes in Cardiovascular Diseases.

Despite years of researches, cardiovascular disease (CVD) remains the most common cause of death around the world. Lots of studies showed that by pretreating with short nonfatal ischemia in in situ organ or distant organ, one could develop tolerance to the following fatal ischemia. The process is called ischemic preconditioning (IPC). IPC prepare the heart for damage by producing inflammatory signals, miRNA, neuro system stimulation and exosomes. Among them, exosomes have been gaining increasing interest since it is characterized by its capability to carry information and its specific ligand-receptor system. Here we will discuss IPC induced exosomes and its protective effects during ischemic heart disease.

miR-19b controls cardiac fibroblast proliferation and migration.

Cardiac fibrosis is a fundamental constituent of a variety of cardiac dysfunction, making it a leading cause of death worldwide. However, no effective treatment for cardiac fibrosis is available. Therefore, novel therapeutics for cardiac fibrosis are highly needed. Recently, miR-19b has been found to be able to protect hydrogen peroxide (H2 O2 )-induced apoptosis and improve cell survival in H9C2 cardiomyocytes, while down-regulation of miR-19b had opposite effects, indicating that increasing miR-19b may be a new therapeutic strategy for attenuating cellular apoptosis during myocardial ischaemia-reperfusion injury. However, considering the fact that microRNAs might exert a cell-specific role, it is highly interesting to determine the role of miR-19b in cardiac fibroblasts. Here, we found that miR-19b was able to promote cardiac fibroblast proliferation and migration. However, miR-19b mimics and inhibitors did not modulate the expression level of collagen I. Pten was identified as a target gene of miR-19b, which was responsible for the effect of miR-19b in controlling cardiac fibroblast proliferation and migration. Our data suggest that the role of miR-19b is cell specific, and systemic miR-19b targeting in cardiac remodelling might be problematic. Therefore, it is highly needed and also urgent to investigate the role of miR-19b in cardiac remodelling in vivo.

Cardiac telocytes are double positive for CD34/PDGFR-α.

Telocytes (TCs) are a distinct type of interstitial cells, which are featured with a small cellular body and long and thin elongations called telopodes (Tps). TCs have been widely identified in lots of tissues and organs including heart. Double staining for CD34/PDGFR-ß (Platelet-derived growth factor receptor ß) or CD34/Vimentin is considered to be critical for TC phenotyping. It has recently been proposed that CD34/PDGFR-α (Platelet-derived growth factor receptor α) is actually a specific marker for TCs including cardiac TCs although the direct evidence is still lacking. Here, we showed that cardiac TCs were double positive for CD34/PDGFR-α in primary culture. CD34/PDGFR-α positive cells (putative cardiac TCs) also existed in mice ventricle and human cardiac valves including mitral valve, tricuspid valve and aortic valve. Over 87% of cells in a TC-enriched culture of rat cardiac interstitial cells were positive for PDGFR-α, while CD34/PDGFR-α double positive cells accounted for 30.25% of the whole cell population. We show that cardiac TCs are double positive for CD34/PDGFR-α. Better understanding of the immunocytochemical phenotypes of cardiac TCs might help using cardiac TCs as a novel source in cardiac repair.

Clinical Outcome of Middle Thoracic Esophageal Cancer with Intrathoracic or Cervical Anastomosis.

BACKGROUNDS: What is the optimal way for the middle esophageal cancer? It is still controversial. In this study, the clinical outcome of middle thoracic esophageal cancer with either intrathoracic or cervical anastomosis was analyzed in our department. PATIENTS AND METHODS: A total of 205 patients who suffered from middle thoracic esophageal cancer were divided into two groups. In group A, 91 patients received intrathoracic anastomosis above aortic arch after esophageal resection via single left thoracotomy, and in group B, 114 patients received cervical anastomosis after esophageal resection via right thoracotomy and median laparotomy. Data of these patients were collected, and morbidity and mortality were analyzed retrospectively. Survival rate was estimated using the Kaplan-Meier method and comparisons between groups were performed with log-rank test. Univariate and multivariate analyses were performed using Cox model to look for independent predictors of survival. RESULTS: Postoperative complications occurred more frequently in group B, such as hemorrhage (p = 0.011), wound infection (p = 0.032), and temporary paresis of the recurrent laryngeal nerve (p = 0.001). Morbidity of anastomotic leak was higher in group B (8.8 vs. 2.2%; p = 0.048), but the associated mortality was not increased. The extent of radical esophagectomy and lymphadenectomy was much greater in group B; therefore, longer esophagus was resected that reduced the cancer residual rate, and more positive lymph nodes were detected that enhanced the accuracy of clinical staging. Fortunately, more patients received adjuvant therapy after operation in group B, and the 5-year survival rate was improved. CONCLUSION: Anastomotic leak rate was higher in cervical anastomosis but with lower mortality. The 5-year survival rate was improved in cervical anastomosis group. The present data support the assumption that cervical anastomosis is a safer and more beneficial procedure for patients with middle thoracic esophageal cancer.

Comparison of thoracolaparoscopic esophagectomy with cervical anastomosis with McKeown esophagectomy for middle esophageal cancer.

BACKGROUND: In China, the middle esophageal squamous cell cancer is the most common tumor type, and Mckeown esophagectomy (ME) is preferably adopted by thoracic surgeon. But, the surgical trauma of ME is great. Thoracolaparoscopic esophagectomy (TE) was developed to decrease the operative stress; however, the safety and efficacy were not defined. In this study, clinical outcomes were compared between patients who received ME and TE. METHODS: The data of 113 patients who suffered from middle-thoracic esophageal cancer during the same period were collected. Sixty-two patients received ME (ME group), and 51 patients received TE (TE group). Patients' demographics and short-term clinicopathologic outcomes were comparable between the two groups. Survival rate was estimated using the Kaplan-Meier method, and comparisons between groups were performed with log-rank test. RESULTS: Patients in TE group had lower body mass index (BMI). Preoperative tumor stage in TE group was much earlier. Both overall and thoracic operation time were longer in TE group. The blood loss during operation and postoperative day (POD) 1 was less in TE group, which contributed to the less blood transfusion. In TE group, postoperative incidence of pulmonary complications and atrial fibrillation (p = 0.035 and p = 0.033) was lower; the inflammatory response and incision pain were significantly alleviated; the ICU and in-hospital stay was shorter as well because of less surgical trauma. No statistically significant difference was found between two groups in terms of overall survival or disease-free survival. CONCLUSIONS: The efficacy and safety of TE were supported by the selected patients in this cohort study. Although it is lack of randomness in this research, some advantages of TE were gratifying such as lower postoperative complications and similar survival with ME. A multicenter prospective randomized study is now required.

Delta mean neutrophil volume (ΔMNV) is comparable to procalcitonin for predicting postsurgical bacterial infection.

BACKGROUND: The Coulter LH750 (Beckman Coulter, Brea, CA) analyzer can determine intrinsic biophysical properties of white blood cell (WBC), known as cell population data. Previous studies have shown that mean neutrophil volume (MNV) was significantly increased in postsurgical patients with bacterial infection. To further validate its potential clinical usefulness, we investigate the changes in MNV before and after surgery, called ΔMNV. We also compare the ΔMNV with procalcitonin (PCT) and C-reactive protein (CRP) in terms of diagnostic sensitivity and specificity for postsurgical bacterial infection. METHODS: Blood samples from 300 healthy controls, 219 cardiac surgical patients without postsurgical infection, and 31 cardiac surgical patients complicated with postsurgical bacterial infection were studied. RESULTS: There are no statistically significant differences for WBC count and neutrophil percentage prior to or after surgery between postsurgical noninfected and infected patients. However, the ΔMNV is significantly increased in postsurgical infected patients when compared with noninfected patients (P < 0.05). The receiver-operating characteristics analysis reveals the ΔMNV and PCT have largest areas under curves (0.92, 0.93 on the second day and 0.94, 0.99 on the third day postsurgery, respectively) compared to other parameters. CONCLUSION: ΔMNV shows comparable sensitivity and specificity to PCT and superior sensitivity and specificity to WBC or CRP for predicting postsurgical bacterial infection. The potential clinical application of this parameter merits further exploration in a larger prospective study.

Identification of 5 hub genes for diagnosis of coronary artery disease.

Background: Coronary artery disease (CAD) is a main cause leading to increasing mortality of cardiovascular disease (CVD) worldwide. We aimed to discover marker genes and develop a diagnostic model for CAD. Methods: CAD-related target genes were searched from DisGeNET. Count expression data and clinical information were screened from the GSE202626 dataset. edgeR package identified differentially expressed genes (DEGs). Using online STRING tool and Cytoscape, protein-protein reactions (PPI) were predicted. WebGestaltR package was employed to functional enrichment analysis. We used Metascape to conduct module-based network analysis. VarElect algorithm provided genes-phenotype correlation analysis. Immune infiltration was assessed by ESTIMATE package and ssGSEA analysis. mRNAsi was determined by one class logistic regression (OCLR). A diagnostic model was constructed by SVM algorithm. Results: 162 target genes were screened by intersection 1,714 DEGs and 1,708 CAD related target genes. 137 target genes of the 162 target genes were obtained using PPI analysis, in which those targets were enriched in inflammatory cytokine pathways, such as chemokine signaling pathway, and IL-17 signaling pathway. From the above 137 target genes, four functional modules (MCODE1-4) were extracted. From the 162 potential targets, CAD phenotype were directly and indirectly associated with 161 genes and 22 genes, respectively. Finally, 5 hub genes (CCL2, PTGS2, NLRP3, VEGFA, LTA) were screened by intersections with the top 20, directly and indirectly, and genes in MCODE1. PTGS2, NLRP3 and VEGFA were positively, while LTA was negatively correlated with immune cells scores. PTGS2, NLRP3 and VEGFA were negatively, while LTA was positively correlated with mRNAsi. A diagnostic model was successfully established, evidenced by 92.59% sensitivity and AUC was 0.9230 in the GSE202625 dataset and 94.11% sensitivity and AUC was 0.9706 in GSE120774 dataset. Conclusion: In this work, we identified 5 hub genes, which may be associated with CAD development.

Microsurgical anatomy of the abducens nerve.

OBJECTIVE: To clarify the oriented classification, relationships, and variations of the abducens nerve and provide a detailed description of its microsurgical anatomic features. METHODS: A microsurgical anatomic dissection of the abducens nerve was performed in 100 specimens obtained from 50 adult cadaveric heads fixed in formalin and two adult cadaveric heads stained with hematoxylin and eosin for histological examination. Important neurovascular and structural relationships of the abducens nerve were observed. RESULTS: The abducens nerve was divided into five segments (cisternal, petroclival, internal carotid artery, fissural, and intraconal). It coursed in the petroclival venous confluence and there was a complex anatomic relationship. Two new types of abducens nerve variations were found. In one type, the duplicated nerve is split into two branches for a limited length in the cavernous sinus (CS). The other is a complex type, which has a complex course and pattern. This type of duplicated abducens nerve has a communicating branch in the cistern and numerous fasciculi in the CS. In addition, the two branches do not accompany each other for the entire course in the CS. CONCLUSION: The vulnerability of the abducens nerve results from diverse factors. The inferolateral trunk, which arises from the intracavernous segment of carotid artery (also called the artery of the inferior CS), is an important landmark for finding the abducens nerve and sympathetic nerve. Variations of the abducens nerve are not rare. Keeping variations of the nerve in mind is important during skull base operations and transvenous endovascular interventions. Understanding the relationship of the abducens nerve with adjacent structures will help us in preparing for safe surgery.

Long Noncoding RNA FAM225A Promotes Esophageal Squamous Cell Carcinoma Development and Progression via Sponging MicroRNA-197-5p and Upregulating NONO.

Esophageal squamous cell carcinoma (ESCC) is the major subclass of esophageal cancer and one of the most life-threatening malignancies with high morbidity and mortality. Long noncoding RNAs (lncRNAs) participate in tumorigenesis and metastasis of various tumors. Here, we investigated the function of a newly identified lncRNA FAM225A in ESCC. LncRNA FAM225A expression was significantly higher in ESCC and predicted poor prognosis of ESCC patients. We confirmed that upregulation of FAM225A in ESCC and overexpression of FAM225A was associated with poor outcome in ESCC patients using TCGA ESCC cohort. Knockdown of FAM225A significantly inhibited cell growth, migration and invasion of ESCC cells in vitro and inhibited ESCC xenograft development in vivo. Mechanistically, we demonstrated that lncRNA FAM225A functioned as a competing endogenous RNA (ceRNA) via sponging miR-197-5p. LncRNA FAM225A exerted its regulatory function on ESCC proliferation and metastasis via modulating expression of miR-197-5p. MiR-197-5p overexpression antagonized the function of FAM225A, with decreased cell growth and invasion. Moreover, we identified that RNA binding protein NONO was a direct target of miR-197-5p and miR-197-5p negatively regulated NONO expression and TGF-ß signaling in ESCC cells. In summary, our findings suggest that lncRNA FAM225A promotes ESCC development and progression via sponging miR-197-5p and upregulating NONO expression. These results suggest that lncRNA FAM225A could be explored as a new therapy target in ESCC treatment.

Upregulation of glucosamine-phosphate N-acetyltransferase 1 is a promising diagnostic and predictive indicator for poor survival in patients with lung adenocarcinoma.

Lung adenocarcinoma, a type of non-small cell lung cancer, is the leading cause of cancer death worldwide. Great efforts have been made to identify the underlying mechanism of adenocarcinoma, especially in relation to oncogenes. The present study by integrating computational analysis with western blotting, aimed to understand the role of the upregulation of glucosamine-phosphate N-acetyltransferase 1 (GNPNAT1) in carcinogenesis. In the present study, publicly available gene expression profiles and clinical data were downloaded from The Cancer Genome Atlas to determine the role of GNPNAT1 in lung adenocarcinoma (LUAD). In addition, the association between LUAD susceptibility and GNPNAT1 upregulation were analyzed using Wilcoxon signed-rank test and logistic regression analysis. In LUAD, GNPNAT1 upregulation was significantly associated with disease stage [odds ratio (OR)=2.92, stage III vs. stage I], vital status (dead vs. alive, OR=1.89), cancer status (tumor status vs. tumor-free status, OR=1.85) and N classification (yes vs. no, OR=1.75). Cox regression analysis and the Kaplan-Meier method were utilized to evaluate the association between GNPNAT1 expression and overall survival (OS) time in patients with LUAD. The results demonstrated that patients with increased GNPNAT1 expression levels exhibited a reduced survival rate compared with those with decreased expression levels (P=8.9×10-5). In addition, Cox regression analysis revealed that GNPNAT1 upregulation was significantly associated with poor OS time [hazard ratio (HR): 1.07; 95% confidence interval (CI): 1.04-1.10; P<0.001]. The gene set enrichment analysis revealed that 'cell cycle', 'oocyte meiosis', 'pyrimidine mediated metabolism', 'ubiquitin mediated proteolysis', 'one carbon pool by folate', 'mismatch repair progesterone-mediated oocyte maturation' and 'basal transcription factors purine metabolism' were differentially enriched in the GNPNAT1 high-expression samples compared with GNPNAT1 low-expression samples. The aforementioned pathways are involved in the pathogenesis of LUAD. The findings of the present study suggested that GNPNAT1 upregulation may be considered as a promising diagnostic and prognostic biomarker in patients with LUAD. In addition, the aforementioned pathways may be pivotal pathways perturbed by the abnormal expression of GNPNAT1 in LUAD. The findings of the present study demonstrated the therapeutic value of the regulation of GNPNAT1 in lung adenocarcinoma.

MiRNA505/NET1 Axis Acts as a CD8+ T-TIL Regulator in Non-Small Cell Lung Cancer.

INTRODUCTION: Lung adenocarcinoma (LUAD), which is the most important and common subtype of non-small cell lung cancer (NSCLC), is highly heterogeneous with a poor prognosis and poses great challenges to health worldwide. MicroRNAs (miRNAs) are regulators of gene expression with recognized roles in physiology and diseases, such as cancers, but little is known about their functional relevance to CD8+ T cell infiltration regulation in the tumor microenvironment (TME) of NSCLC patients, especially LUAD patients. METHODS: Bioinformatic analysis was used to analyze TCGA data. RT-PCT, Western blot, luciferase assay and immunohistochemistry were used to detect the expression levels and bindings of genes and miRNA. ELISA and cytotoxic assay were used to evaluate CD8+ T cell function. RESULTS: In this study, bioinformatic analysis unveiled the miR-505-3p/NET1 pair as a CD8+ T-tumor-infiltrating lymphocyte (TIL) regulator. Then, we confirmed the bioinformatic results with LUAD patient samples, and NET1 was shown to be a direct target of miR-505-3p in a luciferase assay. Functional experiments demonstrated that miR-505-3p enhanced CD8+ T-TIL function, while NET1 impaired CD8+ T-TIL function and partly reversed the effects of miR-505-3p. The observed effects might be exerted via the regulation of immunosuppressive receptors in T cells. DISCUSSION: Our study may provide novel insights into LUAD progression related to the TME mechanism and new possibilities for improving adoptive immunotherapy.

Neuroepithelial Cell Transforming Gene 1 Acts as an Oncogene and Is Mediated by miR-22 in Human Non-Small-Cell Lung Cancer.

Abnormal expression of neuroepithelial cell transforming gene 1 (NET1) has been authenticated in many human cancers, including lung cancer. We have previously reported that NET1 functioned as an oncogene and promoted human non-small-cell lung cancer (NSCLC) growth and migration. However, the correlation between NET1 and its upstream miRNAs needed further illustration. Our present work demonstrated that miR-22 had a relatively low expression, and NET1 had a relatively high expression in both NSCLC samples and lung adenocarcinoma cell lines compared with corresponding normal controls. Moreover, miR-22 directly regulated NET1 and was verified to weaken cancer cell proliferation and migration, as well as enhance cell apoptosis by suppressing NET1. Furthermore, the inhibitory effect of miR-22 can be reversed via overexpressing NET1 using an ectopic expression vector in NSCLC cells. Our findings showed that miR-22/NET-1 axis may contribute to the inhibition of NSCLC growth and migration and represents a promising therapeutic target for NSCLC.