Gene expression profiling after LINC00472 overexpression in an NSCLC cell line

2021 ◽  
pp. 1-14
Author(s):  
Danbi Seo ◽  
Jungwook Roh ◽  
Yeonsoo Chae ◽  
Wanyeon Kim
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Tumor Suppressors ◽  
Enrichment Analysis ◽  
Nsclc Cell Line ◽  
Sequencing Analysis ◽  
Genetic Characteristics ◽  
Migration Assay ◽  
Non Coding Rna ◽  
And Migration

Lung cancer accounts for a large proportion of cancer-related deaths worldwide. Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a long non-coding RNA and has been recently suggested to be a biomarker of NSCLC, but little is known of its mechanism in NSCLC. Thus, the current study was performed to document changes in gene expression after LINC00472 overexpression in NSCLC cells. As a result of cell viability and migration assay, LINC00472 downregulated cell survival, proliferation, and motility. Transcriptome sequencing analysis showed 3,782 genes expression were changed in LINC00472 overexpressing cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed most genes were associated with intracellular metabolism. The PPP1R12B, RGS5, RBM5, RBL2, LDLR and PTPRM genes were upregulated by LINC00472 overexpression and these genes functioned as tumor suppressors in several cancers. In contrast, SPSB1, PCNA, CD24, CDK5, CDC25A, and EIF4EBP1 were downregulated by LINC00472, and they functioned as oncogenes in various cancers. Consequently, the function of LINC00472 in tumorigenesis might be related to changes in the expressions of other oncogenes and tumor suppressors.

scholarly journals Identification of key genes associated with lung adenocarcinoma by bioinformatics analysis

2021 ◽  
Vol 104 (1) ◽  
pp. 003685042199727
Author(s):  
Xinyu Wang ◽  
Jiaojiao Yang ◽  
Xueren Gao
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cox Regression ◽  
Enrichment Analysis ◽  
Tumor Stage ◽  
Gene Expression Omnibus ◽  
Poor Overall Survival ◽  
Key Genes ◽  
Low Expression

Lung adenocarcinoma (LUAD) is the most common histological type of lung cancer, comprising around 40% of all lung cancer. Until now, the pathogenesis of LUAD has not been fully elucidated. In the current study, we comprehensively analyzed the dysregulated genes in lung adenocarcinoma by mining public datasets. Two sets of gene expression datasets were obtained from the Gene Expression Omnibus (GEO) database. The dysregulated genes were identified by using the GEO2R online tool, and analyzed by R packages, Cytoscape software, STRING, and GPEIA online tools. A total of 275 common dysregulated genes were identified in two independent datasets, including 54 common up-regulated and 221 common down-regulated genes in LUAD. Gene Ontology (GO) enrichment analysis showed that these dysregulated genes were significantly enriched in 258 biological processes (BPs), 27 cellular components (CCs), and 21 molecular functions (MFs). Furthermore, protein-protein interaction (PPI) network analysis showed that PECAM1, ENG, KLF4, CDH5, and VWF were key genes. Survival analysis indicated that the low expression of ENG was associated with poor overall survival (OS) of LUAD patients. The low expression of PECAM1 was associated with poor OS and recurrence-free survival of LUAD patients. The cox regression model developed based on age, tumor stage, ENG, PECAM1 could effectively predict 5-year survival of LUAD patients. This study revealed some key genes, BPs, CCs, and MFs involved in LUAD, which would provide new insights into understanding the pathogenesis of LUAD. In addition, ENG and PECAM1 might serve as promising prognostic markers in LUAD.

Signal Transducer and Activator of Transcription6 Signaling Pathway in Tumor-Associated Macrophage Aggravates Lung Cancer Progression

2021 ◽  
Vol 11 (9) ◽  
pp. 1707-1713
Author(s):  
Jun Wan ◽  
Jian Wang ◽  
Qiurong Huang ◽  
Guanggui Ding ◽  
Xiean Ling
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
T Cell ◽  
Cancer Progression ◽  
Cancer Tissue ◽  
M2 Macrophage ◽  
Normal Tissues ◽  
Tumor Associated Macrophage ◽  
M1 Macrophage ◽  
And Migration

Lung cancer is a most common cancer worldwide. Tumor-associated macrophage (TAM) is known a key effector cell in tumor microenvironment. Meanwhile, STAT6 is crucial to cancer development. We aimed to determine the interaction between STAT6 and TAMs in lung cancer. In this work, firstly, we established mouse model of lung cancer. Then, immunofluorescence was performed to determine STAT6 and CD206 level in lung cancer tissue and adjacent normal tissues as well as model mice. RT-qPCR was applied to detect differentiation of macrophage and determine related gene expression. After treatment of siRNA of STAT6 or STAT6 inhibitor (AS1517499), Transwell assay and MTT were used to determine cell proliferation and migration. STAT6 was upregulated in lung cancer tissues while arginase was more active in M2 macrophage rather than M1 macrophage. Transfection of si-STAT6 not only decreased differentiation in M2 macrophage but also inhibited proliferative, migratory and invasive ability of cancer cells while AS1517499 led to reduced tumor growth. STAT6 inhibition caused decreased expression of M2 macrophages. Similarly, intratumoral T cell markers showed that CD8+T cell gene expression and CD4-mediated T cell marker FoxP3 was increased slightly. Taken altogether, macrophage-STAT6 promotes cell migration and proliferation in lung cancer.

scholarly journals Serum MiR-4687-3p Has Potential for Diagnosis and Carcinogenesis in Non-small Cell Lung Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Man Liu ◽  
Qiufang Si ◽  
Songyun Ouyang ◽  
Zhigang Zhou ◽  
Meng Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Validation Cohort ◽  
Kegg Pathway ◽  
Enrichment Analysis ◽  
Small Cell ◽  
Pathway Enrichment Analysis ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
Pathway Enrichment ◽  
And Migration

The lack of a useful biomarker partly contributes to the increased mortality of non-small cell lung cancer (NSCLC). MiRNAs have become increasingly appreciated in diagnosis of NSCLC. In the present study, we used microarray to screen 2,549 miRNAs in serum samples from the training cohort (NSCLC, n = 10; the healthy, n = 10) to discover differentially expressed miRNAs (DEMs). Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) assay was applied to validate the expression level of selected overexpressed DEMs of NSCLC in a validation cohort (NSCLC, n = 30; the healthy, n = 30). Area under the receiver operating characteristic curve (AUC) was performed to evaluate diagnostic capability of the DEMs. The expression of the miRNAs in tissues was analyzed based on the TCGA database. Subsequently, the target genes of the miR-4687-3p were predicted by TargetScan. Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were tested by R software (ClusterProfiler package). NSCLC cells were transfected with inhibitor or mimic to down-regulate or up-regulate the miR-4687-3p level. The function of miR-4687-3p on proliferation, invasion, and migration of lung cancer cells were investigated through CCK-8 and Transwell assays, respectively. In the results, we identified serum miR-4687-3p that provided a high diagnostic accuracy of NSCLC (AUC = 0.679, 95%CI: 0.543–0.815) in the validation cohort. According to the TCGA database, we found that the miR-4687-3p level was significantly higher in NSCLC tissues than in normal lung tissues (p < 0.05). GO and KEGG pathway enrichment analysis showed that postsynaptic specialization and TGF-β signaling pathway were significantly enriched. Down-regulation of miR-4687-3p could suppress the proliferation, invasion, and migration of the NSCLC cells, compared with inhibitor negative control (NC). Meanwhile, overexpression of miR-4687-3p could promote the proliferation, invasion, and migration of the NSCLC cells compared with mimic NC. As a conclusion, our study first discovered that serum miR-4687-3p might have clinical potential as a non-invasive diagnostic biomarker for NSCLC and play an important role in the development of NSCLC.

scholarly journals Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells

2020 ◽  
Vol 47 (9) ◽  
pp. 6879-6886
Author(s):  
Amedeo Ferlosio ◽  
Elena Doldo ◽  
Sara Agostinelli ◽  
Gaetana Costanza ◽  
Federica Centofanti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Nsclc Cell Line ◽  
Related Gene ◽  
Down Regulation ◽  
Mammalian Expression ◽  
H460 Cells ◽  
Cellular Retinol Binding Protein

Abstract In recent years, new treatments with novel action mechanisms have been explored for advanced non-small cell lung cancer (NSCLC). Retinoids promote cancer cell differentiation and death and their trafficking and action is mediated from specific cytoplasmic and nuclear receptors, respectively. The purpose of this study was to investigate the effect of Cellular retinol binding protein-1 (CRBP-1) transfection in H460 human NSCLC cell line, normally not expressing CRBP-1. H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBP-1 gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans Retinoic Acid (atRA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array and results analysed by one-way analysis of variance (ANOVA) or by t-student test. CRBP-1+ showed reduced proliferation and viability in basal condition and after atRA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBP-1+ H460 cells associated to the down-regulation of pAKT/pERK/pEGFR-related genes. In particular, gene array documented the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, p27, Jun. Restoration of CRBP-1 expression in H460 cells reduced proliferation and viability in both basal condition and after atRA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBP-1-related intracellular pathways contribute to counteract NSCLC progression in order to suggest a potential tool to improve efficacy of retinoid anti lung cancer adjuvant therapy.

scholarly journals Revealing Biological Pathways Implicated in Lung Cancer from TCGA Gene Expression Data Using Gene Set Enrichment Analysis

2014 ◽  
Vol 13s1 ◽  
pp. CIN.S13882 ◽  
Author(s):  
Binghuang Cai ◽  
Xia Jiang
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Gene Expression Data ◽  
Lung Squamous Cell Carcinoma ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Expression Data ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Pathway Gene

Analyzing biological system abnormalities in cancer patients based on measures of biological entities, such as gene expression levels, is an important and challenging problem. This paper applies existing methods, Gene Set Enrichment Analysis and Signaling Pathway Impact Analysis, to pathway abnormality analysis in lung cancer using microarray gene expression data. Gene expression data from studies of Lung Squamous Cell Carcinoma (LUSC) in The Cancer Genome Atlas project, and pathway gene set data from the Kyoto Encyclopedia of Genes and Genomes were used to analyze the relationship between pathways and phenotypes. Results, in the form of pathway rankings, indicate that some pathways may behave abnormally in LUSC. For example, both the cell cycle and viral carcinogenesis pathways ranked very high in LUSC. Furthermore, some pathways that are known to be associated with cancer, such as the p53 and the PI3K-Akt signal transduction pathways, were found to rank high in LUSC. Other pathways, such as bladder cancer and thyroid cancer pathways, were also ranked high in LUSC.

scholarly journals A Comparative Study of Mouse Hepatic and Intestinal Gene Expression Profiles under PPARαKnockout by Gene Set Enrichment Analysis

PPAR Research ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Kan He ◽  
Qishan Wang ◽  
Yumei Yang ◽  
Minghui Wang ◽  
Yuchun Pan
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Enrichment Analysis ◽  
Small Cell ◽  
Gene Set Enrichment Analysis ◽  
Small Cell Lung ◽  
Gene Set Enrichment ◽  
Tissue Specific

Gene expression profiling of PPARαhas been used in several studies, but fewer studies went further to identify the tissue-specific pathways or genes involved in PPARαactivation in genome-wide. Here, we employed and applied gene set enrichment analysis to two microarray datasets both PPARαrelated respectively in mouse liver and intestine. We suggested that the regulatory mechanism of PPARαactivation by WY14643 in mouse small intestine is more complicated than in liver due to more involved pathways. Several pathways were cancer-related such as pancreatic cancer and small cell lung cancer, which indicated that PPARαmay have an important role in prevention of cancer development. 12 PPARαdependent pathways and 4 PPARαindependent pathways were identified highly common in both liver and intestine of mice. Most of them were metabolism related, such as fatty acid metabolism, tryptophan metabolism, pyruvate metabolism with regard to PPARαregulation but gluconeogenesis and propanoate metabolism independent of PPARαregulation. Keratan sulfate biosynthesis, the pathway of regulation of actin cytoskeleton, the pathways associated with prostate cancer and small cell lung cancer were not identified as hepatic PPARαindependent but as WY14643 dependent ones in intestinal study. We also provided some novel hepatic tissue-specific marker genes.

scholarly journals Contribution of Neuropilin-1 in Radiation-Survived Subclones of NSCLC Cell Line H1299

2021 ◽  
Vol 43 (3) ◽  
pp. 1203-1211
Author(s):  
Kaori Tsutsumi ◽  
Ayaka Chiba ◽  
Yuta Tadaki ◽  
Shima Minaki ◽  
Takahito Ooshima ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Motility ◽  
Cell Line ◽  
Tumor Cells ◽  
Tube Formation ◽  
Nsclc Cell ◽  
Nsclc Cell Line ◽  
Migration Assay ◽  
Lung Cancer Patients ◽  
Neuropilin 1

Non-small cell lung cancer (NSCLC) is an aggressive lung cancer accounting for approximately 85% of all lung cancer patients. For the patients with Stages IIIA, IIIB, and IIIC, the 5-year survival is low though with the combination with radiotherapy and chemotherapy. In addition, the occurrence of tumor cells (repopulated tumors) that survive irradiation remains a challenge. In our previous report, we subcloned the radiation-surviving tumor cells (IR cells) using the human NSCLC cell line, H1299, and found that the expression of neuropilin-1 (NRP-1) was upregulated in IR cells by the microarray analysis. Here, we investigated the contribution of neuropilin-1 to changes in the characteristics of IR cells. Although there were no differences in angiogenic activity in the tube formation assay between parental and IR cells, the cell motility was increased in IR cells compared to parental cells in the cell migration assay. This enhanced cell motility was suppressed by pretreatment with anti-NRP-1 antibody. Although further studies are necessary to identify other molecules associated with NRP-1, the increase in cellular motility in IR cells might be due to the contribution of NRP-1. Inhibition of NRP-1 would help control tumor malignancy in radiation-surviving NSCLC.

scholarly journals MicroRNA-222 promotes the proliferation and migration of cervical cancer cells

2014 ◽  
Vol 37 (3) ◽  
pp. 131 ◽  
Author(s):  
Yi Sun ◽  
Bo Zhang ◽  
Jiajing Cheng ◽  
Yi Wu ◽  
Fing Xing ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Phosphatase And Tensin Homolog ◽  
Migration Assay ◽  
Tensin Homolog ◽  
Siha Cells ◽  
Non Coding Rna ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Purpose: This study aimed to investigate the role of small non-coding RNA-222 (microRNA-222; miR-222) in the development of cervical cancer (CC). Methods: Normal and CC specimens were obtained from 18 patients. HeLa and SiHa cells were grown in Dulbecco’s modified Eagle’s medium. RT–PCR, Western blot, migration assay, flow cytometry and immunofluorescence microscopy were used for analyses. Results: When compared with normal cervical tissues, miR-222 was upregulated in human CC, and the extent of up-regulation was associated with the extent and depth of CC invasion. Expression of miR-222 was inversely related to the expression of phosphatase and tensin homolog (PTEN) and p27. The reduced the expression of PTEN and p27 by miR-222 in HeLa cells and SiHa cells was associated with increased proliferation and migration of CC cells. The expression of proteins (E-cadherin and paxillin) related to the proliferation and migration was also elevated. Conclusion: MiR-222 plays an important role in the tumorigenesis of CC, possibly by specifically down-regulating p27Kip1 and PTEN. Our findings suggest that miR-222 may serve as a new therapeutic target in CC.

scholarly journals MicroRNAs-Role in Lung Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Małgorzata Guz ◽  
Adolfo Rivero-Müller ◽  
Estera Okoń ◽  
Agnieszka Stenzel-Bembenek ◽  
Krzysztof Polberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Heart Disease ◽  
Tumor Suppressors ◽  
Untranslated Region ◽  
Regulation Of Gene Expression ◽  
Noncoding Rnas ◽  
Neoplastic Transformation ◽  
Complementary Sequences ◽  
Tumorigenic Potential

Regulation of gene expression is essential for normal physiological functions; thus deregulation of gene expression is common in disease conditions. One level of regulation of gene expression is performed by noncoding RNAs, among which microRNAs (miRNA) are the best studied. Abnormal expression of these molecular players can lead to pathogenic processes such as heart disease, immune system abnormalities, and carcinogenesis, to name but a few. Of a length of 18–25 nucleotides miRNAs are involved in binding partial complementary sequences within the 3′-UTR (3′-untranslated region) of the target mRNAs. Depending on the type of neoplastic transformation, miRNAs can act both as oncogenes (oncomirs) or as tumor suppressors. Because of the great importance of miRNAs, most researches focus on either their role as biomarkers or their potential as therapeutic targets. Herein, we present the review of microRNA biology, function, and tumorigenic potential with emphasis on their role in lung cancer.

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