miR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells

Duan, Jun; Zhang, Xiaoying; Zhang, Sheng; Shen, Hua; Feng, Zhichun

doi:10.3892/etm.2017.4430

Cited by 20 publications

(10 citation statements)

References 35 publications

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“…Our data also suggested that cis-regulated target genes were involved in the initiation and progression of ESCC. For instance, FN1 is highly expressed in a variety of tumor tissues including ESCC, which can promote tumor metastasis and invasion 22–24 . In our data, FN1 was found to be highly expressed in ESCC tissues (FC = 11.5).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma

Xiao

Tian

et al. 2019

Sci Rep

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Esophageal cancer (EC) is a serious malignancy and that is the fifth leading cause of cancer-related death worldwide. Esophageal squamous cell carcinoma (ESCC) is the main subtype of EC in China. In recent years, long non-coding RNAs (lncRNAs) have demonstrated to be novel tumor-associated regulatory factors. However, the functions and mechanisms of lncRNAs in ESCC have not been fully understood. In this study, we attempted to construct Genome-wide expression profiles of lncRNAs and their potential functions in ESCC. By using microarray, we found a total of 2,366 lncRNAs (1,032 upregulated and 1,334 downregulated) and 3,052 mRNAs (1,477 upregulated and 1,575 downregulated) were differentially expressed between the paired five ESCC tumor tissues and adjacent normal esophageal tissues (fold change, FC ≥2.0 or ≤0.5, p ≤ 0.05). Eight lncRNAs were detected by qRT-PCR to verify the results of the microarray, and the clinicopathological parameters were analyzed in 53 patients with ESCC. GO analysis and KEGG pathway analysis showed that the main biological functions of these abnormal lncRNAs were related to immune response, extracellular vesicular exosome, and protein binding. At the same time, the cis and trans models were used to analyze the potential synergistic regulatory relationship between lncRNAs and their potential target genes. Related genes were the processes that affect cell growth, differentiation, and migration. Then we mapped the lncRNAs-mRNAs co-expression pattern by calculating the PCCs of each lncRNA and mRNA expression value. Furthermore, we investigated the function and potential mechanism of a novel highly expressed lncRNA, lnc-KIAA1244-2, and found that its expression is associated with tumor size, N classification and clinical stage. Knockdown of lnc-KIAA1244-2 inhibited the cell proliferation and inhibited the TNFAIP3 expression in Eca-109 cells. Taken together, the expression patterns of lncRNAs and mRNAs in ESCC tumor tissues are different from those in normal adjacent tissues, and some abnormal expressed lncRNAs may play important roles in the development and progression of ESCC. Lnc-KIAA1244-2 could promote the cell proliferation of ESCC cells and might be a potent therapeutic target for ESCC.

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Section: Discussionmentioning

confidence: 99%

Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma

Xiao

Tian

et al. 2019

Sci Rep

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“…miRNA-206 (miR-206) is a multifunctional miRNA, that is widely involved in various pathological and physiological processes in different tissues. For example, miR-206 was involved in the development of bronchoalveolar dysplasia by down-regulating fibronectin 1 in premature infants with the disease (8). It also downregulates brain-derived neurotrophic factor expression leading to neurological dysfunction of airway smooth muscle, which in turn causes lung inflammatory disease (9).…”

Section: Introductionmentioning

confidence: 99%

miR‑206 regulates alveolar type�II epithelial cell Cx43 expression in sepsis‑induced acute lung injury

Hou

et al. 2019

Exp Ther Med

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The present study investigated the relationship between connexin 43 (Cx43) expression in alveolar type II epithelial cells (ATII) and alveolar air-blood barrier permeability, and the effect of microRNA-206 (miR-206) on the expression of Cx43 in sepsis-induced acute lung injury. For the in vivo study, rats were divided into the sham, caecum ligation and perforation (CLP), CLP+Cx43 inhibitors (Cx43-In) and CLP+miR-206 analogs (miR-206-Mi) groups. CLP method was used to prepare an acute lung injury model of sepsis. Following successful modeling, lung tissue was collected for hematoxylin and eosin (HE) staining, and the wet to dry weight ratio (W/D) and protein content in bronchoalveolar lavage fluid (BALF) were detected. Cx43 expression in lung tissue was determined by immunohistochemistry and western blot analysis. Additionally, miR-206 and Cx43 expression levels in lung tissue were detected by reverse transcription-quantitative polymerase chain reaction. Rat ATII cells were cultured in Transwells plates to form monolayers, then treated with Cx43 mRNA inhibitors or miR-206 analogs. The cell monolayers were then stimulated with lipopolysaccharide and their permeability was evaluated by detecting fluorescein-labeled dextran at the lower chamber of the Transwells. The dual luciferase reporter gene assay was used to investigate whether miR-206 targeted the 3′ untranslated region of Cx43 mRNA to regulate Cx43 expression, thereby regulating the permeability of the alveolar air-blood barrier. Results demonstrated that the CLP method induced damage to the alveolar structure, thickened the alveolar wall, caused hyperemia and hemorrhage in the pulmonary interstitium and caused infiltration of inflammatory cells. Edema in the pulmonary interstitium and alveolar space, exudation of neutrophilic granulocyte and pink edema fluid in alveolar cavities were also observed. W/D ratio, the BALF protein content, and expression of Cx43mRNA and Cx43 were increased significantly, whilst miR-206 expression decreased compared with the control group. The lung tissue inflammatory response was attenuated, and the W/D ratio and BALF protein content decreased in the Cx43-In and miR-206-Mi groups compared with the CLP group. Moreover, Cx43 mRNA and protein expression were decreased significantly in the Cx43-In and miR-206-Mi groups. In addition, the dual luciferase reporter gene assay determined that the untranslated region of Cx43 mRNA had a complementary sequence to miR-206. Of note, Cx43 mRNA expression in the miR-206-Mi group was not significantly decreased in vitro . In conclusion, the increase in ATII cell Cx43 expression during sepsis-induced acute lung injury resulted in an increase in the permeability of the alveolar air-blood barrier. miR-206 targeted the Cx43 mRNA 3′untranslated region to downregulate Cx43 expression, which further improved the permeability of the alveolar air-blood barrier.

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“…To further investigate the underlying molecular role of FN1, we used the miRNA databases (TargetScan, miRDB, and DIANA Tools) to predict the miRNAs that target FN1, and we identi ed the crossings between the results of the three databases, namely miR-429,miR-144-3p,miR-1-3p,miR-1271-5p,miR-206, and miR-96-5p. Afterward, we searched these six miRNAs in PubMed and noticed that four of them have been experimentally veri ed to target FN1, namely miR-429(23),miR-144-3p(24),miR-1271-5p (25) and miR-206 (26). Therefore, further experimental studies about miR-1-3p and miR-96-5p are needed to be con rmed.…”

Section: Discussionmentioning

confidence: 99%

Identification and Verification of Candidate Genes Regulating Human Umbilical Vein Endothelial Cells Behavior Under Hyperglycemia

Ma¹,

Zhou²,

Xie³

et al. 2020

Preprint

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Background: Diabetes is a metabolic disease that has been widely demonstrated to be correlated with many microvascular and macrovascular diseases that seriously damage the patient’s life quality. This study intended to investigate the underlying molecular mechanisms of endothelial dysfunction under hyperglycemia. Methods: The gene expression profile of GSE49524 was downloaded and differentially expressed genes (DEGs) in hyperglycemia human umbilical cord endothelial cells (HUVECs) samples compared with normoglycemia HUVECs samples were identified by R software. Afterward, we analyzed the data by applying a combination of the bioinformatics method and used the microRNAs (miRNAs) databases to predict microRNAs that target key genes. The expression of the top 10 differentially expressed genes was validated through quantitative real-time PCR (qRT-PCR). Results: A total of 65 genes were distinguished as DEGs. The dominant GO (gene ontology) terms and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways which were significantly overrepresented in the hyperglycemia HUVECs were identified. The results of the protein-protein interaction networks demonstrated that fibronectin 1 (FN1) is of the highest degree. In addition, several predicted miRNAs that target FN1 were obtained too. The further verification of the top 10 DEGs through qRT-PCR illustrated that nine of the up-regulated DEGs were up-regulated significantly in the hyperglycemia group when compared to the control group. Conclusions:This exploratory study may help to prompt an understanding of the underlying molecular mechanisms of the effect of hyperglycemia on the behavior of HUVECs and contribute to the production of effective therapeutic interventions.

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miR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells

Cited by 20 publications

References 35 publications

Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma

Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma

miR‑206 regulates alveolar type�II epithelial cell Cx43 expression in sepsis‑induced acute lung injury

Identification and Verification of Candidate Genes Regulating Human Umbilical Vein Endothelial Cells Behavior Under Hyperglycemia

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