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Microarray analysis of differentially expressed long non-coding RNAs in daidzein-treated lung cancer cells.

ABSTRACT: Daidzein has been found to significantly inhibit the proliferation of lung cancer cells, while its potential molecular mechanisms remain unclear. To determine the molecular mechanism of daidzein on lung cancer cells, the Capital Bio Technology Human long non-coding (lnc) RNA Array v4, 4×180K chip was used to detect the gene expression profiles of 40,000 lncRNAs and 34,000 mRNAs in a human cancer cell line. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect the expression levels of target lncRNA and mRNAs in the H1299 cells treated with and without daidzein, using the lncRNA and mRNA gene chip. Bioinformatics analysis was performed to determine the differentially expressed genes from the results of the chip assays. There were 119 and 40 differentially expressed lncRNAs and mRNAs, respectively, that had a 2-fold change in expression level. A total of eight lncRNAs were upregulated in the H1299 lung cancer cells, while 111 lncRNAs were downregulated. Furthermore, five mRNAs were upregulated, and 35 mRNAs were downregulated. A total of six differentially expressed lncRNAs (ENST00000608897.1, ENST00000444196.1, ENST00000608741.1, XR_242163.1, ENST00000505196.1 and ENST00000498032.1) were randomly selected to validate the microarray data, which were consistent with the RT-qPCR analysis results. Differentially expressed mRNAs were enriched in important Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. Taken together, the results of the present study demonstrated that daidzein affected the expression level of lncRNAs in lung cancer cells, suggesting that daidzein may have potential effects on lung cancer cells.

SUBMITTER: Li L

PROVIDER: S-EPMC8488333 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Microarray analysis of differentially expressed long non-coding RNAs in daidzein-treated lung cancer cells

Project description:Daidzein has been found to significantly inhibit the proliferation of lung cancer cells, while its potential molecular mechanisms remain unclear. To determine the molecular mechanism of daidzein on lung cancer cells, the Capital Bio Technology Human long non-coding (lnc)RNA Array v4, 4x180K chip was used to detect the gene expression profiles of 40,000 lncRNAs and 34,000 mRNAs in a human cancer cell line. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect the expression levels of target lncRNA and mRNAs in the H1299 cells treated with and without daidzein, using the lncRNA and mRNA gene chip. Bioinformatics analysis was performed to determine the differentially expressed genes from the results of the chip assays. There were 119 and 40 differentially expressed lncRNAs and mRNAs, respectively, that had a 2-fold change in expression level. A total of eight lncRNAs were upregulated in the H1299 lung cancer cells, while 111 lncRNAs were downregulated. Furthermore, five mRNAs were upregulated, and 35 mRNAs were downregulated. A total of six differentially expressed lncRNAs (ENST00000608897.1, ENST00000444196.1, ENST00000608741.1, XR_242163.1, ENST00000505196.1 and ENST00000498032.1) were randomly selected to validate the microarray data, which were consistent with the RT-qPCR analysis results. Differentially expressed mRNAs were enriched in important Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. Taken together, the results of the present study demonstrated that daidzein affected the expression level of lncRNAs in lung cancer cells, suggesting that daidzein may have potential effects on lung cancer cells.

2021-08-05 | GSE181093 | GEO

Microarray analysis of differentially expressed long non-coding RNAs in daidzein-treated lung cancer cells

Project description:Microarray analysis of differentially expressed long non-coding RNAs in daidzein-treated lung cancer cells

| PRJNA750676 | ENA

Comprehensive analysis of differentially expressed long non-coding RNAs in non-small cell lung cancer.

Project description:Non-small cell lung cancer (NSCLC) is the primary subtype of lung cancer. Long non-coding RNAs (lncRNAs) have been reported to serve prominent roles in cancer progression. However, the expression patterns and potential roles of lncRNAs in NSCLC remain to be elucidated. In the present study, four public datasets were analyzed to identify differentially expressed lncRNAs (DElncs) in NSCLC. A further dataset, GSE19188, was analyzed to validate the findings. A total of 38 upregulated and 31 downregulated lncRNAs were identified in NSCLC, compared with samples from healthy controls. Among these, 12 lncRNAs were associated with the progression of NSCLC, and dysregulated between high grade (stage III and IV) and low grade (stage II) NSCLC samples. Moreover, dysregulation of lncRNA-SIGLEC17P, GGTA1P, A2M-AS1, LINC00938, GVINP1, LINC00667 and TMPO-AS1 was associated with overall survival time in patients with NSCLC. Co-expression analyses, combined with the construction of protein-protein interaction networks, were performed to reveal the potential roles of key lncRNAs in NSCLC. The present study revealed a series of lncRNAs involved in the progression of NSCLS, which may serve as novel biomarkers for the disease.

| S-EPMC6607379 | biostudies-literature

Identification of Differentially Expressed Long Non-coding RNAs in Polarized Macrophages.

Project description:Macrophages display remarkable plasticity, with the ability to undergo dynamic transition between classically and alternatively activated phenotypes. Long non-coding RNAs (lncRNAs) are more than 200 nucleotides in length and play roles in various biological pathways. However, the role of lncRNAs in regulating macrophage polarization has yet to be explored. In this study, lncRNAs expression profiles were determined in human monocyte-derived macrophages (MDMs) incubated in conditions causing activation toward M(IFN-? + LPS) or M(IL-4) phenotypes. Compared with primary MDMs, 9343 lncRNAs and 5903 mRNAs were deregulated in M(IFN-? + LPS) group (fold change ? 2.0, P < 0.05), 4592 lncRNAs and 3122 mRNAs were deregulated in M(IL-4) group. RT-qPCR results were generally consistent with the microarray data. Furthermore, we found that TCONS_00019715 is expressed at a higher level in M(IFN-? + LPS) macrophages than in M(IL-4) macrophages. TCONS_00019715 expression was decreased when M(IFN-? + LPS) converted to M(IL-4) whereas increased when M(IL-4) converted to M(IFN-? + LPS). Knockdown of TCONS_00019715 following the activation of THP-1 cellls using IFN-? and LPS diminished the expression of M(IFN-? + LPS) markers, and elevated the expression of M(IL-4) markers. These data show a significantly altered lncRNA and mRNA expression profile in macrophages exposure to different activating conditions. Dysregulation of some of these lncRNAs may play important roles in regulating macrophage polarization.

| S-EPMC4726337 | biostudies-other

Transcriptional profiling of differentially expressed long non-coding RNAs in breast cancer.

Project description:Long non-coding RNAs (lncRNAs) are subclass of noncoding RNAs that have been recently shown to play critical roles in cancer biology. However, little is known about their mechanistic role in breast cancer pathogenesis, especially in triple-negative breast carcinomas (TNBC) that have particular poor outcomes. This study was specifically designed to identify the signatures relevant lncRNAs in breast cancer and characterize lncRNAs that modulate the phenotype. Here we provide detailed methods and analysis of microarray data, which is deposited in the Gene Expression Omnibus (GEO) with the accession number GSE64790. The basic analysis as contained in the manuscript published in Oncotarget with the PMID 26078338. These data can be used to further elucidate the mechanisms of breast cancer.

| S-EPMC4664755 | biostudies-literature

Long Non-coding RNAs Are Differentially Expressed After Different Exercise Training Programs.

Project description:BackgroundMolecular regulation related to the health benefits of different exercise modes remains unclear. Long non-coding RNAs (lncRNAs) have emerged as an RNA class with regulatory functions in health and diseases. Here, we analyzed the expression of lncRNAs after different exercise training programs and their possible modes of action related to physical exercise adaptations.MethodsPublic high-throughput RNA-seq data (skeletal muscle biopsies) were downloaded, and bioinformatics analysis was performed. We primarily analyzed data reports of 12 weeks of resistance training (RT), high-intensity interval training (HIIT), and combined (CT) exercise training. In addition, we analyzed data from 8 weeks of endurance training (ET). Differential expression analysis of lncRNAs was performed, and an adjusted P-value < 0.1 and log2 (fold change) ≥0.5 or ≤-0.5 were set as the cutoff values to identify differentially expressed lncRNAs (DELs).ResultsWe identified 204 DELs after 12 weeks of HIIT, 43 DELs after RT, and 15 DELs after CT. Moreover, 52 lncRNAs were differentially expressed after 8 weeks of ET. The lncRNA expression pattern after physical exercise was very specific, with distinct expression profiles for the different training programs, where few lncRNAs were common among the exercise types. LncRNAs may regulate molecular responses to exercise, such as collagen fibril organization, extracellular matrix organization, myoblast and plasma membrane fusion, skeletal muscle contraction, synaptic transmission, PI3K and TORC regulation, autophagy, and angiogenesis.ConclusionFor the first time, we show that lncRNAs are differentially expressed in skeletal muscle after different physical exercise programs, and these lncRNAs may act in various biological processes related to physical activity adaptations.

| S-EPMC7533564 | biostudies-literature

Microarray expression profile of long non-coding RNAs in human lung adenocarcinoma.

Project description:BackgroundLong non-coding RNAs (lncRNAs) participate in many biological dynamics and play significant roles in gene regulation. LncRNA expression is altered in many cancers; however, the expressions and functions of lncRNA genes in lung adenocarcinoma (LAD) remain unknown.MethodsLncRNA and messenger RNA (mRNA) expression in LAD without lymphatic metastasis versus paired adjacent non-tumor (ANT) lung tissues and LAD with versus without lymphatic metastasis were analyzed using Human LncRNA Arraystar V3.0. The expression levels of four downregulated and four upregulated lncRNAs were verified using quantitative real-time PCR in cells and tissue specimens.ResultsIn this study, 949 lncRNAs and 681 mRNAs had differential expression in LAD without lymphatic metastasis compared to ANT lung tissues, while 2740 lncRNAs and 1714 mRNAs were differentially expressed in LAD with lymphatic metastasis compared to LAD without lymphatic metastasis. The expression patterns of selected lncRNAs (LINC00113, AC005009.1, ARHGAP22-IT1, AC009411.1, SRGAP3-AS2, EGFEM1P, FAM66E, and HLA-F-AS1) were consistent with microarray data. Differentially expressed mRNA genes were enriched in crucial Gene Ontology terms and pathways.ConclusionOur results revealed differentially expressed lncRNAs in LAD, suggesting lncRNAs may be potential indicators for LAD diagnosis and therapy.

| S-EPMC6166069 | biostudies-literature

Screening and identification of differentially expressed long non-coding RNAs in multidrug-resistant tuberculosis.

Project description:BackgroundEfforts to eradicate tuberculosis are largely threatened by drug-resistant tuberculosis, particularly, multidrug-resistant tuberculosis (MDR-TB). Screening and identification potential biomarkers for MDR-TB is crucial to diagnose early and reduce the incidence of MDR-TB.MethodsTo screen the differentially expressed long non-coding RNAs in MDR-TB, the lncRNA and mRNA expression profiles in serum derived from healthy controls (HCs), individuals with MDR-TB and drug-sensitive tuberculosis (DS-TB) were analyzed by microarray assay and 10 lncRNAs were randomly selected for further validation by reverse transcription-quantitative real-time PCR(RT-qPCR). The biological functions of differentially expressed mRNAs as well as relationships between genes and signaling pathways were investigated using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG), respectively.ResultsA total of 353 differentially expressed lncRNAs (312 upregulated) and 202 mRNAs (99 upregulated) were found in the MDR-TB group compared to HCs. And compared with the DS-TB group, 442 differentially expressed lncRNAs (115 upregulated) and 190 mRNAs (87 upregulated) were found in the MDR-TB group. The expression levels of lncRNA n335659 were found to differ significantly between each group by RT-qPCR. Compared with DS-TB group, the GO analysis showed that the differential mRNAs were mainly enriched in the processes associated with the detection of the chemical stimulus, the regulation of mRNA metabolic process and neutrophil activation in the MDR-TB group; the KEGG analysis indicated that the differential mRNAs between DS-TB and MDR-TB were mainly enriched in proteasome and Notch signaling pathway, which might reveal a fraction of the mechanism of MDR-TB. The discovery of the serum lncRNA n335659 might serve as a potential biomarker for MDR-TB and Notch signaling pathway provided a new clue for the investigation of the pathological mechanism of MDR-TB.

| S-EPMC8772445 | biostudies-literature

Identification of Long Non-coding and Messenger RNAs Differentially Expressed Between Primary and Metastatic Melanoma.

Project description:Purpose: Melanoma is the most aggressive and life-threatening cutaneous cancer. To explore new treatment strategies, it is essential to identify the mechanisms underlying melanoma tumorigenesis and metastasis. Methods: In the current study, we demonstrated altered expression of long non-coding RNA (lncRNA) and messenger RNA (mRNA) in melanoma using data from the Cancer Genome Atlas (TCGA) database. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction (PPI) analyses were conducted. We also constructed a functional lncRNA-mRNA regulatory network and Kaplan-Meier analysis. Results: We identified 246 differentially expressed (DE) lncRNAs and 856 DEmRNAs. A total of 184 DElncRNAs and 428 DEmRNAs were upregulated in metastatic melanoma, while all others were downregulated. Additionally, we investigated the co-expression pattern of 363 genes, among which 26 upregulated lncRNAs, 9 down- regulated lncRNAs, 49 upregulated mRNAs and 151 downregulated mRNAs were identified as being co-expressed with others. Survival analysis suggested high levels of 14 lncRNAs and 10 mRNAs may significantly increase or decrease overall survival. These differentially expressed genes are also potentially prognostic in melanoma. Conclusion: Our findings observe potential roles for lncRNAs and mRNAs during melanoma progression and provide candidate biomarkers for further studies.

| S-EPMC6459964 | biostudies-literature

Analysis of differentially expressed long non-coding RNAs in LPS-induced human HMC3 microglial cells.

Project description:BackgroundLong non-coding RNAs (lncRNAs) are emerging as key modulators of inflammatory gene expression, but their roles in neuroinflammation are poorly understood. Here, we identified the inflammation-related lncRNAs and correlated mRNAs of the lipopolysaccharide (LPS)-treated human microglial cell line HMC3. We explored their potential roles and interactions using bioinformatics tools such as gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG), and weighted gene co-expression network analysis (WGCNA).ResultsWe identified 5 differentially expressed (DE) lncRNAs, 4 of which (AC083837.1, IRF1-AS1, LINC02605, and MIR3142HG) are novel for microglia. The DElncRNAs with their correlated DEmRNAs (99 total) fell into two network modules that both were enriched with inflammation-related RNAs. However, treatment with the anti-inflammatory agent JQ1, an inhibitor of the bromodomain and extra-terminal (BET) protein BRD4, neutralized the LPS effect in only one module, showing little or even enhancing effect on the other.ConclusionsThese results provide insight into, and a resource for studying, the regulation of microglia-mediated neuroinflammation and its potential therapy by small-molecule BET inhibitors.

| S-EPMC9795738 | biostudies-literature

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