Biological pathway analysis by ArrayUnlock and Ingenuity Pathway Analysis

Jiménez-Marín, Ángeles; Collado-Romero, Melania; Ramírez-Boo, M.; Arce, Cristina; Garrido, Juan J.

doi:10.1186/1753-6561-3-s4-s6

Cited by 133 publications

(103 citation statements)

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“…The microarray data was processed with the edgeR package to analyze differential expression of genes 13. Ingenuity pathway analysis (IPA) software (Qiagen, Redwood City, CA) was used for analysis of the signaling and metabolic pathways, molecular networks, and biological processes most significantly perturbed in the gene expression datasets 14. IPA was also used to predict TFs, which could be responsible for gene expression changes and whether those TFs are activated or inhibited in EMT.…”

Section: Methodsmentioning

confidence: 99%

Transcriptome profiling reveals novel gene expression signatures and regulating transcription factors of TGFβ‐induced epithelial‐to‐mesenchymal transition

Yamamoto

Burnette

et al. 2016

Cancer Medicine

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Dysregulated epithelial to mesenchymal transition (EMT) in cancer cells endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs and therefore play a critical role in transforming early‐stage carcinomas into invasive malignancies. EMT has also been associated with tumor recurrence and drug resistance and cancer stem cell initiation. Therefore, better understanding of the mechanisms behind EMT could ultimately contribute to the development of novel prognostic approaches and individualized therapies that specifically target EMT processes. As an effort to characterize the central transcriptome changes during EMT, we have developed a Transforming growth factor (TGF)‐beta‐based in vitro EMT model and used it to profile EMT‐related gene transcriptional changes in two different cell lines, a non‐small cell lung cancer cell line H358, and a breast cell line MCF10a. After 7 days of TGF‐beta/Oncostatin M (OSM) treatment, changes in cell morphology to a mesenchymal phenotype were observed as well as concordant EMT‐associated changes in mRNA and protein expression. Further, increased motility was noted and flow cytometry confirmed enrichment in cancer stem cell‐like populations. Microarray‐based differential expression analysis identified an EMT‐associated gene expression signature which was confirmed by RT‐qPCR and which significantly overlapped with a previously published EMT core signature. Finally, two novel EMT‐regulating transcription factors, IRF5 and LMCD1, were identified and independently validated.

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Section: Methodsmentioning

confidence: 99%

Transcriptome profiling reveals novel gene expression signatures and regulating transcription factors of TGFβ‐induced epithelial‐to‐mesenchymal transition

Yamamoto

Burnette

et al. 2016

Cancer Medicine

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“…Their relative changes and annotation are listed in table 4. Functional annotation and pathway interaction of these genes was done using the BABELOMICS platform [16] and ingenuity pathways analysis (IPA) [17]. Gene ontology annotation of three of the 20 genes remained unestablished.…”

Section: Resultsmentioning

confidence: 99%

Malignant pleural effusion cells show aberrant glucose metabolism gene expression

et al. 2010

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Malignant pleural effusion (MPE) accompanying lung adenocarcinoma indicates poor prognosis and early metastasis. This study aimed to identify genes related to MPE formation.Three tissue sample cohorts, seven from healthy lungs, 18 from stage I-III lung adenocarcinoma with adjacent healthy lung tissue and 13 from lung adenocarcinomas with MPE, were analysed by oligonucleotide microarray. The identified genes were verified by quantitative realtime PCR (qRT-PCR), immunohistochemical staining, and immunofluorescence confocal microscopy.20 up-or down-regulated genes with a two-fold change in MPE cancer cells compared to healthy tissues were differentially expressed from early-to late-stage lung cancer. Of 13 genes related to cellular metabolism, aldolase A (ALDOA), sorbitol dehydrogenase (SORD), transketolase (TKT), and tuberous sclerosis 1 (TSC1) were related to glucose metabolism. qRT-PCR validated their mRNA expressions in pleural metastatic samples. Immunohistochemical staining confirmed aberrant TKT, ALDOA, and TSC1 expressions in tumour cells. Immunofluorescence confirmed TKT co-localisation and co-distribution of ALDOA with thyroid transcription factor 1-positive cancer cells. TKT regulated the proliferation, vascular endothelial growth factor secretion in vitro and in vivo vascular permeability of cancer cell.Glucose metabolic reprogramming by ALDOA, SORD, TKT and TSC1 is important in MPE pathogenesis.

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“…This analysis tool generated networks and pathways in which the differentially regulated genes could be related according to previously known associations between genes or proteins, but independently of established canonical pathways. 40 The graphic representation of the miR-21 target network was generated using the network visualization tool embedded in Cytoscape. 41 Functional classification of CSF-1R-regulated miR-21 targets based on Gene Ontology terms was performed using CSF-1 stimulation, preparation of cell lysates, and western blotting Subconfluent (;70%) 100-mm tissue culture dishes of macrophages were CSF-1-starved for 16 hours to upregulate CSF-1R expression.…”

Section: Microarrays Bioinformatics Analysis and Statisticsmentioning

confidence: 99%

Colony stimulating factor-1 receptor signaling networks inhibit mouse macrophage inflammatory responses by induction of microRNA-21

Caescu

Guo

Tesfa³

et al. 2015

Blood

134

118

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Key Points• Analysis of CSF-1R pTyrregulated messenger RNAs identifies novel signaling nodes and networks that can be targeted to modulate macrophage functions.• miR-21 is a novel CSF-1R pTyr-721-induced molecule that suppresses the macrophage M1 phenotype and enhances the M2 phenotype.Macrophage polarization between the M2 (repair, protumorigenic) and M1 (inflammatory) phenotypes is seen as a continuum of states. The detailed transcriptional events and signals downstream of colony-stimulating factor 1 receptor (CSF-1R) that contributes to amplification of the M2 phenotype and suppression of the M1 phenotype are largely unknown. Macrophage CSF-1R pTyr-721 signaling promotes cell motility and enhancement of tumor cell invasion in vitro. Combining analysis of cellular systems for CSF-1R gain of function and loss of function with bioinformatic analysis of the macrophage CSF-1R pTyr-721-regulated transcriptome, we uncovered microRNA-21 (miR-21) as a downstream molecular switch controlling macrophage activation and identified extracellular signal-regulated kinase 1/2 and nuclear factor-kB as CSF-1R pTyr-721-regulated signaling nodes. We show that CSF-1R pTyr-721 signaling suppresses the inflammatory phenotype, predominantly by induction of miR-21. Profiling of the miR-21-regulated messenger RNAs revealed that 80% of the CSF-1-regulated canonical miR-21 targets are proinflammatory molecules. Additionally, miR-21 positively regulates M2 marker expression. Moreover, miR-21 feeds back to positively regulate its own expression and to limit CSF-1R-mediated activation of extracellular signal-regulated kinase 1/2 and nuclear factor-kB. Consistent with an anti-inflammatory role of miRNA-21, intraperitoneal injection of mice with a miRNA-21 inhibitor increases the recruitment of inflammatory monocytes and enhances the peritoneal monocyte/macrophage response to lipopolysaccharide. These results identify the CSF-1R-regulated miR-21 network that modulates macrophage polarization. (Blood. 2015;125(8):e1-e13) IntroductionMacrophages protect the host against infection and injury and facilitate tissue remodeling.1 However, they frequently accumulate in pathological settings, including cancers, 2 atherosclerosis, 3 metabolic disease, 4 and sepsis, 5 where they respond to microenvironmental cues that can be detrimental to the host. Two distinct extreme states of polarized activation have been described in macrophages:6,7 the classically activated (M1) and the alternatively activated (M2) macrophage phenotypes, each characterized by well-described markers. 5,6,[8][9][10][11] M1 macrophages produce proinflammatory cytokines, elevate the expression of inducible nitric oxide synthase 2 (iNOS) and major histocompatibility complex class II (MHC II), 12 and can play antitumorigenic roles. 5,9 In contrast, the M2 macrophages have increased expression of scavenger receptors, increased activation of the arginase pathway, low expression of interleukin-12 (IL-12), high expression of IL-10 and IL-1RA, and increased anti-inflammatory responses a...

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Biological pathway analysis by ArrayUnlock and Ingenuity Pathway Analysis

Cited by 133 publications

References 1 publication

Transcriptome profiling reveals novel gene expression signatures and regulating transcription factors of TGFβ‐induced epithelial‐to‐mesenchymal transition

Transcriptome profiling reveals novel gene expression signatures and regulating transcription factors of TGFβ‐induced epithelial‐to‐mesenchymal transition

Malignant pleural effusion cells show aberrant glucose metabolism gene expression

Colony stimulating factor-1 receptor signaling networks inhibit mouse macrophage inflammatory responses by induction of microRNA-21

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