Influence of electrohydrodynamics on the drying characteristics and volatile components of iron stick yam.

The drying characteristics, rehydration capacity, color, infrared spectra and volatile components of iron stick yam slices were investigated under different alternating current (AC) voltages (13, 17, 21 kV), hot air drying (HAD) (60 °C) and natural drying (AD) by electrohydrodynamic (EHD) drying and HAD experimental devices. The results showed that slices of iron stick yam dried the quickest with HAD, which also had the fastest drying rate; while drying the slices of iron stick yam with EHD led to a better rehydration capacity, higher brightness L* and whiteness, a more stable protein secondary structure, and a greater variety and content of volatile components compared with AD and HAD. These finding indicated that EHD is a more promising method for drying iron stick yam.

Dietary Supplementation of Brevibacillus laterosporus S62-9 Improves Broiler Growth and Immunity by Regulating Cecal Microbiota and Metabolites.

Brevibacillus laterosporus has been added as a direct-fed microbiota to chicken. Yet, few studies have reported the effects of B. laterosporus on broiler growth and gut microbiota. The aim of this study was to evaluate the effects of B. laterosporus S62-9 on growth performance, immunity, cecal microbiota, and metabolites in broilers. A total of 160 1-day-old broilers were randomly divided into S62-9 and control groups, with or without 106 CFU/g B. laterosporus S62-9 supplementation, respectively. During the 42 days feeding, body weight and feed intake were recorded weekly. Serum was collected for immunoglobulin determination, and cecal contents were taken for 16S rDNA analysis and metabolome at Day 42. Results indicated that the broilers in S62-9 group showed an increase in body weight of 7.2% and 5.19% improvement in feed conversion ratio compared to the control group. The B. laterosporus S62-9 supplementation promoted the maturation of immune organs and increased the concentration of serum immunoglobulins. Furthermore, the α-diversity of cecal microbiota was improved in the S62-9 group. B. laterosporus S62-9 supplementation increased the relative abundance of beneficial bacteria including Akkermansia, Bifidobacterium, and Lactobacillus, while decreased the relative abundance of pathogens including Klebsiella and Pseudomonas. Untargeted metabolomics revealed that 53 differential metabolites between the two groups. The differential metabolites were enriched in 4 amino acid metabolic pathways, including arginine biosynthesis and glutathione metabolism. In summary, B. laterosporus S62-9 supplementation could improve the growth performance and immunity through the regulation of gut microbiota and metabolome in broilers.

[Retracted] MicroRNA­629 inhibition suppresses the viability and invasion of non­small cell lung cancer cells by directly targeting RUNX3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell invasion assays in Figs. 4D and 5D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 3933­3940, 2019; DOI: 10.3892/mmr.2019.9990].

Upregulation of circ_0059961 suppresses cholangiocarcinoma development by modulating miR-629-5p/SFRP2 axis.

BACKGROUND: Cholangiocarcinoma (CCA) is a dangerous malignancy with a poor prognosis due to inefficient chemotherapy and surgery, and its pathophysiology could be linked to circular RNA (circRNAs) dysregulation. As a result, we wanted to see what role circ_0059961 plays in CCA. METHODS: The quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of circ_0059961, miR-629-5p, and secreted frizzled related protein 2 (SFRP2). Cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (Edu) assay were used to determine the role of circ_0059961 in proliferation. The MMP (Δψm) assay was used to assess cell apoptosis. Transwell assay was used to detect cell migration and invasion. The SFRP2 protein and epithelia-mesenchymal transition (EMT) process related proteins expression were measured using Western blot. The putative relationship between miR-629-5p and circ_0059961 or SFRP2 was validated by dual-luciferase reporter assay. The circ_0059961 roles in cholangiocarcinoma were also investigated by tumor xenograft assay. RESULTS: Circ_0059961 expression was decreased in CCA tissues and carcinoma cells. Overexpressed circ_0059961 reduced tumor cell proliferation, migration, and invasion while inducing apoptosis. Circ_0059961 was proven to be a target of miR-629-5p, while miR-629-5p was confirmed to be a target of SFRP2. Circ_0059961 targeted miR-629-5p to modulate SFRP2 expression. Upregulation of miR-629-5p reversed the tumor-suppressive effects of circ_0059961 overexpression in rescue trials. Furthermore, SFRP2 overexpression restored miR-629-5p enrichment-promoted cell proliferation, migration, and invasion. Upregulated circ_0059961 reduced solid tumor growth in vivo. CONCLUSION: Upregulation of circ_0059961 augmented SFRP2 expression by targeting miR-629-5p, which blocked cholangiocarcinoma tumor cell proliferation, migration, and invasion.

MicroRNA-629-3p Promotes Interleukin-13-Induced Bronchial Epithelial Cell Injury and Inflammation by Targeting FOXA2.

OBJECTIVE: Asthma is a chronic pulmonary inflammatory disease. MicroRNA (miR)-629-3p expression is reported to be up-regulated in the sputum of asthma patients. Nonetheless, miR-629-3p's role and mechanism in asthma remain largely unknown. This study is aimed at exploring miR-629-3p's role in regulating the injury and inflammation of bronchial epithelial cells. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression levels of miR-629-3p and forkhead box a2 (FOXA2) mRNA in 16HBE cells treated with interleukin-13 (IL-13). 16HBE cell viability was evaluated using the cell counting kit-8 (CCK-8) assay, and cell apoptosis was analyzed by a flow cytometer. The levels of C-C motif chemokine ligand 11 (CCL11), C-C motif chemokine ligand 26 (CCL26), C-C motif ligand 2 (CCL-2)/mono-cyte chemotactic protein-1 (MCP-1), interleukin-1 beta (IL-1b), and interleukin 6 (IL-6) in 16HBE cell supernatant were detected through enzyme-linked immunosorbent assay (ELISA). The downstream target genes of miR-629-3p were predicted through bioinformatics. Besides, the targeted relationship between miR-629-3p and FOXA2 mRNA 3'-UTR was verified by dual-luciferase reporter gene assay. Western blot was utilized to determine the regulatory effects of miR-629-3p on the expression of FOXA2 protein in 16HBE cells. RESULTS: MiR-629-3p expression was significantly enhanced in IL-13-stimulated 16HBE cells while the FOXA2 mRNA and protein levels were significantly down-regulated. The transfection of miR-629-3p mimics inhibited 16HBE cells' viability, and promoted the apoptosis and the secretion of chemokines CCL11, CCL26, CCL-2/MCP-1, IL-1b, and IL-6 of 16HBE cells, whereas inhibiting miR-629-3p had the opposite effects. Moreover, FOXA2 was identified as a downstream miR-629-3p target, and its overexpression reversed the effects of the miR-629-3p on 16HBE cells. CONCLUSION: MiR-629-3p promotes IL-13-induced 16HBE cells' injury and inflammation by targeting FOXA2.

MiR-629-5p Promotes Prostate Cancer Development and Metastasis by Targeting AKAP13.

Prostate cancer (PCa) has become the most frequently occurring cancer among western men according to the latest report, and patients' prognosis is often poor in the event of tumor progression, therefore, many researches are devoted to exploring the molecular mechanism of PCa metastasis. MicroRNAs (miRNA) have proved to play an important role in this process. In present study, by combining clinical samples with public databases, we found that miR-629-5p increased to varying degrees in primary localized PCa tissues and metastatic PCa tissues compared with adjacent normal tissues, and bioinformatics analysis suggested that high level of miR-629-5p was related to poor prognosis. Functionally, miR-629-5p drove PCa cell proliferation, migration and invasion in vitro, and promoted growth of PCa cells in vivo. Moreover, A-kinase Anchor Protein 13 (AKAP13) was screened as a direct target of miR-629-5p, that expression was negatively correlated with the malignant phenotype of tumor cells. In the end, through verification in clinical specimens, we found that AKAP13 could be independently used as a clinical prognostic indicator. Overall, the present study indicates that miR-629-5p plays an oncogenic role in PCa by targeting AKAP13, which provides a new idea for clinical diagnosis and treatment of complex refractory PCa.

Overexpression of Long Non-Coding RNA MIR22HG Represses Proliferation and Enhances Apoptosis via miR-629-5p/TET3 Axis in Osteosarcoma Cells.

In this study, we evaluated the mechanism of long non-coding RNA MIR22 host gene (LncRNA MIR22HG) in osteosarcoma cells. Forty-eight paired osteosarcoma and adjacent tissues samples were collected and the bioinformatic analyses were performed. Target genes and potential binding sites of MIR22HG, microRNA (miR)-629-5p and tet methylcytosine dioxygenase 3 (TET3) were predicted by Starbase and TargetScan V7.2 and confirmed by dual-luciferase reporter assay. Cell Counting Kit-8, colony formation and flow cytometry assays were utilized to determine the viability, proliferation and apoptosis of transfected osteosarcoma cells. Pearson's analysis was introduced for the correlation analysis between MIR22HG and miR-629-5p in osteosarcoma tissue. Relative expressions of MIR22HG, miR-629-5p and TET3 were measured by quantitative real-time polymerase chain reaction or Western blot. MiR-629-5p could competitively bind with and was negatively correlated with MIR22HG, the latter of which was evidenced by the high expression of miR-629-5p and low expression of MIR22HG in osteosarcoma tissues. Overexpressed MIR22HG repressed the viability and proliferation but enhanced apoptosis of osteosarcoma cells, which was reversed by miR-629-5p upregulation. TET3 was the target gene of miR-629-5p, and the promotive effects of upregulated miR-629-5p on the viability and proliferation as well as its repressive effect on apoptosis were abrogated via overexpressed TET3. To sum up, overexpressed MIR22HG inhibits the viability and proliferation of osteosarcoma cells, which was achieved via regulation of the miR-629-5p/TET3 axis.

Comparative Whole Genome Analysis of Escherichia coli O157:H7 Isolates From Feedlot Cattle to Identify Genotypes Associated With the Presence and Absence of stx Genes.

A comparative whole genome analysis was performed on three newly sequenced Escherichia coli O157:H7 strains with different stx profiles, previously isolated from feedlot cattle [C1-010 (stx1-, stx2c+), C1-057 (stx-), and C1-067 (stx1+, stx2a+)], as well as five foodborne outbreak strains and six stx-negative strains from NCBI. Phylogenomic analysis demonstrated that the stx2c-carrying C1-010 and stx-negative C1-057 strains were grouped with the six NCBI stx-negative E. coli O157:H7 strains in Cluster 1, whereas the stx2a-carrying C1-067 and five foodborne outbreak strains were clustered together in Cluster 2. Based on different clusters, we selected the three newly sequenced strains, one stx2a-carrying strain, and the six NCBI stx-negative strains and identify their prophages at the stx insertion sites. All stx-carrying prophages contained both the three Red recombination genes (exo, bet, gam) and their repressor cI. On the other hand, the majority of the stx-negative prophages carried only the three Red recombination genes, but their repressor cI was absent. In the absence of the repressor cI, the consistent expression of the Red recombination genes in prophages might result in more frequent gene exchanges, potentially increasing the probability of the acquisition of stx genes. We further investigated each of the 10 selected E. coli O157:H7 strains for their respective unique metabolic pathway genes. Seven unique metabolic pathway genes in the two stx2a-carrying strains and one in the single stx2c-carrying and seven stx-negative strains were found to be associated with an upstream insertion sequence 629 within a conserved region among these strains. The presence of more unique metabolic pathway genes in stx2a-carrying E. coli O157:H7 strains may potentially increase their competitiveness in complex environments, such as feedlot cattle. For the stx2c-carrying and stx-negative E. coli O157:H7 strains, the fact that they were grouped into the same phylogenomic cluster and had the same unique metabolic pathway genes suggested that they may also share closely related evolutionary pathways. As a consequence, gene exchange between them is more likely to occur. Results from this study could potentially serve as a basis to help develop strategies to reduce the prevalence of pathogenic E. coli O157:H7 in livestock and downstream food production environments.

LncRNA MAGI2-AS3 acts as a tumor suppressor that attenuates non-small cell lung cancer progression by targeting the miR-629-5p/TXNIP axis.

BACKGROUND: Lung cancer is a malignant tumor that seriously threatens the health of human beings. Long non-coding RNAs (lncRNAs) are thought to play important roles in the pathophysiology of lung cancer. In this study, we identified a new lncRNA, MAGI2-AS3 in non-small cell lung cancer (NSCLC) tissues by conducting an integrated bioinformatics analysis. Mechanistic studies were also performed to explore the biological functions of MAGI2-AS3 in NSCLC progression. METHODS: A bioinformatics analysis was conducted to determine the prognostic role of MAGI2-AS3. CCK-8, EdU assay, colony formation and Transwell were performed to determine the effects of MAGI2-AS3 on the progression of NSCLC cells. A nude mice model was used to evaluate the effects of MAGI2-AS2 on the in vivo tumor growth of NSCLC. Luciferase reporter and RNA pull-down assays were used to evaluate interactions between MAGI2-AS3 and its downstream targets. RESULTS: MAGI2-AS3 was found to be downregulated in NSCLC tissues. The gain-of-function in vitro studies showed that the overexpression of MAGI2-AS3 suppressed NSCLC cell proliferation and invasion. Conversely, the knockdown of MAGI2-AS3 had the opposite effects. The bioinformatics analysis and luciferase report assay revealed that MAGI2-AS3 functioned as competing endogenous RNA to suppress microRNA (miR)-629-5p expression, while miR-629-5p suppressed thioredoxin-interacting protein (TXNIP) expression by targeting its 3' untranslated region. The rescue experiment results showed that MAGI2-AS3 knockdown enhanced NSCLC cell progression (increasing cell proliferation and invasion, but reducing cell apoptosis), which was counteracted by miR-629-5p inhibition or TXNIP overexpression. CONCLUSIONS: The study revealed that MAGI2-AS3 was downregulated in NSCLC tissues and cells, and MAGI2-AS3 suppressed NSCLC cell progression. Further, the mechanistic results showed that MAGI2-AS3 exerted a tumor-suppressive effect in NSCLC by targeting the miR-629-5p/TXNIP axis.

MicroRNA-629-5p promotes osteosarcoma proliferation and migration by targeting caveolin 1

Osteosarcoma is a highly malignant tumor that occurs in the bone. Previous studies have shown that multiple microRNAs (miRNAs) regulate the development of osteosarcoma. This study aimed to explore the role of miR-629-5p and its target gene, caveolin 1 (CAV1), in osteosarcoma development. To analyze the expression of miR-629-5p and CAV1 mRNA in osteosarcoma tissues and cell lines, qRT-PCR analysis was performed. Dual-luciferase reporter experiments were subsequently performed to validate the relationship between CAV1 and miR-629-5p. CCK8 assay was used to measure osteosarcoma cell proliferation, and wound-healing assay was performed to study their migratory phenotype. Our findings revealed that miR-629-5p was overexpressed in osteosarcoma tissues and cells, and thereby enhanced cell proliferation and migration. Further, we validated that miR-629-5p targets CAV1 mRNA directly. CAV1 expression, which was negatively correlated with miR-629-5p expression, was found to be downregulated in osteosarcoma tissue samples. Moreover, our data showed that an increase in CAV1 level led to a decline in osteosarcoma cell proliferation and migration, which could be rescued by miR-629-5p upregulation. Overall, our study confirmed that miR-629-5p promoted osteosarcoma proliferation and migration by directly inhibiting CAV1.

Antibacterial mechanism of brevilaterin B: an amphiphilic lipopeptide targeting the membrane of Listeria monocytogenes.

Antimicrobial peptides (AMPs) are recognized as promising safe alternatives to antibiotics for its low drug-resistance. Brevilaterin B, a newly discovered antimicrobial lipopeptide produced by Brevibacillus laterosporus S62-9, exhibits efficient antibacterial activity on Listeria monocytogenes with a minimum inhibitory concentration of 1 µg mL-1. The present research aimed to investigate the antibacterial mechanism of brevilaterin B against Listeria monocytogenes. Brevilaterin B caused membrane depolarization and the breakup of the cytomembrane as measured by 3,3-dipropylthiadicarbocyanine iodide and transmission electron microscopy, respectively. Using 1,2-dipalmitoyl-sn-glycero-3-phosphocholine and 1,2-dipalmitoyl-sn-glycero-3-phospho-rac-(1-glycerol) sodium salt (7:3) as a model membrane, results proved that brevilaterin B could bind to liposomes, integrate into the lipid bilayer, and consequently increase the permeability of liposomes to calcein. The secondary structure of brevilaterin B also changed from an unstructured coil to a mainly ß-sheet conformation as measured by circular dichroism. Brevilaterin B exhibits antibacterial activity by a membrane interaction mechanism, which provides a theoretical basis for using brevilaterin B as a promising natural and effective antimicrobial agent against pathogenic bacteria. KEY POINTS: • Brevilaterin B exhibited antibacterial activity against Listeria monocytogenes. • Brevilaterin B exhibited membrane interaction mechanism. • Brevilaterin B showed conformational change when interacted with liposome.

MicroRNA-629 promotes the tumorigenesis of non-small-cell lung cancer by targeting FOXO1 and activating PI3K/AKT pathway.

OBJECTIVE: MicroRNA-629 (miR-629) has been found to play an important role in the pathogenesis of human cancers. However, the function of miR-629 is still unknown in non-small-cell lung cancer (NSCLC). The purpose of this study is to preliminarily elucidate the regulatory mechanism of miR-629 in NSCLC. MATERIALS AND METHODS: The mRNA and protein expression was measured by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. The function of miR-629 was investigated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and Transwell assays. The relationship between miR-629 and FOXO1 was confirmed by dual luciferase assay. RESULTS: MiR-629 was upregulated in NSCLC tissues and cells. High expression of miR-629 predicted poor prognosis in patients with NSCLC. Moreover, miR-629 promoted cell proliferation, migration and invasion in NSCLC cells. In addition, FOXO1 was confirmed as a direct target of miR-629 in NSCLC. Furthermore, knockdown of FOXO1 also promoted proliferation, migration and invasion of NSCLC cells. More importantly, overexpression of FOXO1 weakened the carcinogenesis of miR-629 in NSCLC. Besides that, miR-629 promoted EMT and activated the PI3K/AKT pathway in NSCLC. CONCLUSIONS: MiR-629 promotes the progression of NSCLC by targeting FOXO1 and regulating EMT/PI3K/AKT pathway.

MYCT1 inhibits the EMT and migration of laryngeal cancer cells via the SP1/miR-629-3p/ESRP2 pathway.

MYCT1 has an inhibitory effect on the migration of laryngeal cancer cells, although the underlying molecular mechanism remains unknown. In this study, we aimed to explore the mechanism of MYCT1 in the epithelial-mesenchymal transition (EMT) and migration of laryngeal cancer cells. We found that MYCT1 significantly decreased the expression of miR-629-3p but increased the expression of ESRP2 in laryngeal cancer cells. The expression of miR-629-3p and ESRP2 in laryngeal cancer tissues showed significantly positive and negative correlations with patient metastasis, respectively. miR-629-3p was confirmed to repress the expression of ESRP2 by targeting its 3'UTR. SP1 was verified to be a direct transcription factor for miR-629-3p and a downstream target of MYCT1. Moreover, MYCT1 inhibited the EMT and migration of laryngeal cancer cells through the SP1/miR-629-3p/ESRP2 pathway. Taken together, our results establish a novel MYCT1 signaling pathway in the EMT and migration of laryngeal cancer cells, thus providing important insights for further studying the pathway in the diagnosis and treatment of laryngeal cancer.

CD44s Induces miR-629-3p Expression in Association with Cisplatin Resistance in Head and Neck Cancer Cells.

Cisplatin (cis-diamminedichloroplatinum II [CDDP] ) is a well-known chemotherapeutic drug that has been used for the treatment of various types of human cancers, including head and neck cancer. Cisplatin exerts anticancer effects by causing DNA damage, replication defects, transcriptional inhibition, cell cycle arrest, and the induction of apoptosis. However, drug resistance is one of the most serious problems with cancer chemotherapy, and it causes expected therapeutic effects to not always be achieved. Here, we analyzed global microRNA (miRNA) expression in CD44 standard form (CD44s)-expressing SAS cells, and we identified miR-629-3p as being responsible for acquiring anticancer drug resistance in head and neck cancer. The introduction of miR-629-3p expression inhibited apoptotic cell death under cisplatin treatment conditions, and it promoted cell migration. Among the computationally predicted target genes of miR-629-3p, we found that a number of gene expressions were suppressed by the transfection with miR-629-3p. Using a xenografting model, we showed that miR-629-3p conferred cisplatin resistance to SAS cells. Clinically, increased miR-629-3p expression tended to be associated with decreased survival in head and neck cancer patients. In conclusion, our data suggest that the increased expression of miR-629-3p provides a mechanism of cisplatin resistance in head and neck cancer and may serve as a therapeutic target to reverse chemotherapy resistance.

Elevated Expression of miR-629 Predicts a Poor Prognosis and Promotes Cell Proliferation, Migration, and Invasion of Osteosarcoma.

PURPOSE: Osteosarcoma (OS) is an invasive bone tumor that primarily affects children and adolescents. MicroRNA-629 (miR-629) acts as an oncogene involved in the development of various cancers. This study aims to reveal the clinical significance and biological function of miR-629 in OS. PATIENTS AND METHODS: The levels of miR-629 expression in tissues and cells were detected through quantitative real-time polymerase chain reaction (qRT-PCR). Chi-square test was used to evaluate the relationship between miR-621 expression and clinical parameters in patients with OS. Survival analysis was performed by the Kaplan-Meier method. Cox regression analysis of the effect of miR-629 expression on the prognosis of OS patients. CCK-8 and Transwell experiments were used to demonstrate the effect of miR-629 on OS cell function. RESULTS: Compared with the controls, miR-629 levels were significantly elevated in patients with OS (P < 0.001), Furthermore, miR-629 upregulation showed significantly associated with clinical stage (P = 0.011), distant metastasis (P = 0.003) and poor survival (log rank test, P = 0.013) in OS patients. miR-629 might be a potential prognostic biomarker for OS (HR = 2.890, 95% CI = 1.126-7.416, P = 0.027). Cell function experiments proved that the high expression of miR-629 promoted cell proliferation, migration, and invasion of OS. CONCLUSION: All experimental results demonstrated that miR-629 as an oncogene promotes the tumor cell growth, migration and invasion of OS, and miR-629 may act as a novel prognostic biomarker and therapeutic target for patients with this malignant tumor.

miR-629 targets FOXO3 to promote cell apoptosis in gastric cancer.

Gastric cancer (GC) is one of the most aggressive types of human tumor worldwide, and the 5-year survival rate is less than 25%. The transcriptional factor, forkhead box O3 (FOXO3), is regulated by various micro (mi)RNAs and has been reported to be associated with multiple regulatory signaling pathways involved in tumor development. The current study therefore assessed the impact of miR-629 and FOXO3 on gastric cancer. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to assess the expression of mRNA and protein, respectively. Additionally, the cell proliferation and apoptosis rate were determined via an MTT assay and flow cytometry, respectively. The online database TargetScan predicted that FOXO3 was a target of miR-629. A luciferase reporter assay was also performed to verify that FOXO3 was the direct target of miR-629. The results demonstrated that miR-629 and FOXO3 was upregulated and downregulated in GC tissue, respectively. Furthermore, following transfection with a miR-629 inhibitor, SGC-7901, cell proliferation and apoptosis rate were inhibited and promoted when compared with the control group, respectively. Moreover, after the treatment with SGC-7901, the expression of FOXO3, Bax, Caspase 3 was upregulated, and Bcl-2 was downregulated. Furthermore, the luciferase reporter assay revealed that FOXO3 was the target of miR-629. The results demonstrated that miR-629 and FOXO3 serve vital roles in the development of gastric cancer and may be a future therapeutic target.

MiR-629-3p-induced downregulation of SFTPC promotes cell proliferation and predicts poor survival in lung adenocarcinoma.

The long-term prognosis of patients with lung cancer remains poor and thus it is imminent to further elucidate the molecular mechanism for the oncogenesis of lung cancer. In this study, we observed that surfactant protein C (SFTPC) expression was downregulated in human lung adenocarcinoma tissues and cell lines, and low SFTPC expression correlated with poor overall survival of lung adenocarcinoma patients. Moreover, we found that overexpression of SFTPC could inhibit lung cancer cell proliferation in vitro and in vivo, but downregulation of SFTPC showed the opposite results. Besides, it was observed that miR-629-3p expression was upregulated in human lung adenocarcinoma tissues and cell lines. More importantly, we found that miR-629-3p could downregulate SFTPC expression by directly binding to the SFTPC 3'-UTR and inhibit the regulatory effect of SFTPC on lung adenocarcinoma cell proliferation. In conclusion, these data suggested that miR-629-3p-meditated downregulation of SFTPC may promote lung adenocarcinoma progression.

MiR-629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP.

Pulmonary arterial hypertension (PAH) is featured by the increase in pulmonary vascular resistance and pulmonary arterial pressure. Despite that abnormal proliferation and phenotypic changes in human pulmonary artery smooth muscle cells (HPASMCs) contributing to the pathophysiology of PAH, the underlying molecular mechanisms remain unclear. In the present study, we detected the expression of miR-629 in hypoxia-treated HPASMCs and explored the mechanistic role of miR-629 in regulating HPASMC proliferation, migration and apoptosis. Hypoxia time-dependently induced up-regulation of miR-629 and promoted cell viability and proliferation in HPASMCs. Treatment with miR-629 mimics promoted HPASMCs proliferation and migration, but inhibited cell apoptosis; while knockdown of miR-629 suppressed the cell proliferation and migration but promoted cell apoptosis in HPASMCs. The bioinformatics prediction revealed FOXO3 and PERP as downstream targets of miR-629, and miR-629 negatively regulated the expression of FOXO3 and PERP via targeting the 3' untranslated regions. Enforced expression of FOXO3 or PERP attenuated the miR-629 overexpression or hypoxia-induced enhanced effects on HPASMC proliferation and proliferation, and the suppressive effects on HPASMC apoptosis. Furthermore, the expression of miR-629 was up-regulated, and the expression of FOXO3 and PERP mRNA was down-regulated in the plasma from PAH patients when compared to healthy controls. In conclusion, the present study provided evidence regarding the novel role of miR-629 in regulating cell proliferation, migration and apoptosis of HPASMCs during hypoxia.

miR-629-5p promotes growth and metastasis of hepatocellular carcinoma by activating ß-catenin.

Aberrant miR-629-5p expression in several cancer types has been reported. Nonetheless, its potential effect and mechanism of action on tumor growth and metastasis in hepatocellular carcinoma (HCC) have rarely been analyzed. In this study, we found that miR-629-5p was upregulated in HCC tissue samples as compared to matched adjacent-tissue samples. Overexpression of miR-629-5p promoted the proliferation, migration, and invasiveness of human HCC cells in vitro, whereas miR-629-5p knockdown reduced these parameters. Consistently, miR-629-5p overexpression accelerated tumor growth and metastasis in a nude mouse model. Mechanistically, miR-629-5p directly targeted the 3' untranslated region (3'UTR) of the secreted frizzled-related protein 2 (SFRP2) mRNA and suppressed its expression, resulting in the activation of ß-catenin. Inhibition of ß-catenin abrogated miR-629-5p-induced growth and invasiveness. Collectively, these results suggest that miR-629-5p activates ß-catenin signaling by downregulating SFRP2 and thus promotes the growth and metastasis of HCC. These data open up new prospects for HCC treatment.

Immunomodulatory effects of chicken egg yolk antibodies (IgY) against experimental Shewanella marisflavi AP629 infections in sea cucumbers (Apostichopus japonicus).

Skin ulceration syndrome in sea cucumbers is an infectious bacterial disease with fast and high mortality. This study investigated the protection of chicken egg yolk antibodies (IgY) on skin ulcer syndrome in sea cucumbers induced by intraperitoneally injecting Shewanella marisflavi AP629. Inactivated whole S. marisflavi AP629 cells were used as an immunogen to immunize laying hens. The highest titer of the obtained specific IgY by ELISA was 1:90000. Specific IgY significantly inhibited the growth of S. marisflavi AP629 in a liquid medium, dose-dependent manner at concentrations ranging from 0.5 to 2 mg/mL. Results obtained from scanning electron microscopy and confocal laser scanning microscopy showed that specific IgY could make bacteria agglutinate and damage the cell membrane of S. marisflavi AP629, resulting in a decrease of bacterial viability. Sea cucumbers treated with 25, 5, and 1 mg/mL anti-S. marisflavi AP629 IgY could achieve survival rates of 77.5%, 50%, and 22.5% at day 12 when the infection and injection therapy were carried out at the same time, respectively. However, survival rates of sea cucumbers treated with 25 mg/mL of nonspecific IgY were only 7.5% at day 12. All sea cucumbers in the positive control group died within twelve days after bacterial inoculation. Levels of the five humoral immune factors (LYZ, ACP, NOS, SOD, CAT) released by coelomocytes were significantly increased in the specific IgY group compared to the nonspecific IgY and positive control groups within 12 h. However, the activities of LYZ, ACP, and SOD decreased rapidly at the 48 h time point in the specific IgY group, indicating that specific IgY treatment could shorten the time needed to restore balance in sea cucumber immune systems. Oral prophylaxis with egg yolk powders was that all sea cucumbers were challenged with 4.2 × 106 CFU S. marisflavi AP629 by intraperitoneal injection after 60 days of feeding. Survival rates of diets containing 10%, 5%, and 1% specific egg yolk powder were 57.5%, 52.5%, and 30% by day 12, respectively, and the survival rate was 27.5% for the nonspecific group and 22.5% for the positive control group. After feeding for 60 days, enzyme activities of LZY, NOS, and SOD were all significantly enhanced in sea cucumbers fed with specific egg yolk powder when compared to the control group (p < 0.05). This study demonstrated that the phagocytic activities of coelomocytes were significantly stimulated after specific IgY treatment over that of nonspecific IgY or without IgY treatments in sea cucumbers (p < 0.05). Overall, our results revealed that anti-S. marisflavi AP629 IgY has a positive immunomodulatory effect on sea cucumbers infected with S. marisflavi AP629.