Identification of differentially expressed genes regulated by molecular signature in breast cancer-associated fibroblasts by bioinformatics analysis

Vastrad, Basavaraj; Vastrad, Chanabasayya; Tengli, Anandkumar; Iliger, Sudhir

doi:10.1007/s00404-017-4562-y

Cited by 8 publications

(8 citation statements)

References 136 publications

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“…Although the biological importance of STAMBP in development has been recognized because the microcephaly–capillary malformation syndrome is caused by its somatic mutations, studies of its role in carcinogenesis are limited. In a protein–protein interaction analysis, breast cancer‐associated fibroblast samples had downregulation of STAMBP expression …”

Section: Discussionmentioning

confidence: 99%

Prediagnostic circulating inflammation biomarkers and esophageal squamous cell carcinoma: A case–cohort study in Japan

Aversa

Song

Shimazu³

et al. 2019

Intl Journal of Cancer

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Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer worldwide. Measurements of circulating inflammation-related biomarkers may inform etiology or provide noninvasive signatures for early diagnosis. We therefore examined levels of inflammation molecules for associations with ESCC risk. Using a case-cohort study designed within the Japan Public Health Center-based Prospective Study, we measured baseline plasma levels of 92 biomarkers using a multiplex assay in a subcohort of 410 randomly selected participants and 66 participants with incident ESCC (including four cases that occurred in the subcohort). ESCC hazard ratios (HRs) were calculated for 2-4 quantiles of each biomarker by Cox proportional hazards regression models with age as the time metric, adjusted for sex, smoking and alcohol use. Twenty analytes were undetectable in nearly all samples. Of the remaining 72, 12 biomarkers (FGF19, ST1A1, STAMBP, AXIN1, CASP8, NT3, CD6, CDCP1, CD5, SLAMF1, OPG and CSF1) were associated with increased ESCC risk (p trend < 0.05) with HRs per quantile 1.28-1.65. Seven biomarkers (CXCL6, CCL23, CXCL5, TGFA, CXCL1, OSM and CCL4) were inversely associated with HRs 0.57-0.72. FGF19, CASP8, STAMBP, ST1A1 and CCL-4 met statistical significance with false discovery rate correction. Associations did not differ <5 vs. ≥5 years between blood collection and ESCC diagnosis. CASP8, STAMBP and ST1A1 were strongly correlated (p < 0.05). Our study expands the range of inflammation molecules associated with the development of this highly lethal neoplasia. Correlations among these novel biomarkers suggest a possible shared pathway. These findings need replication and could further delineate ESCCs molecular mechanisms of carcinogenesis.Additional Supporting Information may be found in the online version of this article.

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Section: Discussionmentioning

confidence: 99%

Prediagnostic circulating inflammation biomarkers and esophageal squamous cell carcinoma: A case–cohort study in Japan

Aversa

Song

Shimazu³

et al. 2019

Intl Journal of Cancer

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“…The up-regulated and down-regulated DEGs were obtained at first, and then GSEA analysis was processed. Several pathways including extracellular space [ 7 ], extracellular region [ 8 ], plasma membrane [ 9 ], and integral component of plasma membrane [ 10 ] were closely associated with tumor genesis, growth and metastasis. Loom et al investigated that extracellular space was an important compartment for malignant energetic catalysis and therapeutic targeting [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Key genes affecting the progression of nasopharyngeal carcinoma identified by RNA-sequencing and bioinformatic analysis

Wang

Guo

et al. 2021

Aging

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Background: The present work was conducted to screen the potential biomarkers affecting nasopharyngeal carcinoma (NPC) progression through RNA-sequencing (RNA-seq), bioinformatic analysis and functional experiments. Materials and Methods: Six normal samples and five NPC clinical samples were collected for RNA-seq analysis. The expression levels in both groups were determined through student’s t -test. We identified genes of P < 0.01 as the differentially expressed genes (DEGs). In addition, gene set enrichment analysis (GSEA) was conducted. Afterwards, STRING V10 database was employed to extract protein interactions among the DEGs. Later, we established a protein-protein interaction (PPI) network, and used the Cytoscape software for network visualization. qRT-PCR was conducted to verify hub genes from clinical samples. Then, the function of CXCL10 in cell proliferation, apoptosis, invasion and migration was evaluated. Results: A total of 2024 DEGs were identified, among which, 1449 were down-regulated and 575 were up-regulated. The PPI was constructed, and the hub genes including Insulin Like Growth Factor 1 ( IGF1 ), C-X-C Motif Chemokine Ligand 10 ( CXCL10 ), Interleukin 13 ( IL13 ), Intercellular Adhesion Molecule 1 ( ICAM1 ), G Protein Subunit Gamma Transducin 1 ( GNGT1 ), Matrix Metallopeptidase 1 ( MMP1 ), Neurexin 1 ( NRXN1 ) and Matrix Metallopeptidase 3 ( MMP3 ) were obtained. The expression levels of CXCL10, IGF1, MMP3, MMP1, ICAM1, and IL-13 were significantly up-regulated in tumor tissues. High expression levels of CXCL10, MMP3 and ICAM1 predicted poor prognosis of NPC patients. CXCL10 silencing suppressed NPC cell proliferation and migration. Conclusions: CXCL10 may serve as a potential key gene affecting NPC genesis and progression.

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“…Significant similarities were detected between ALD hHSCs and alcohol‐activated mHSCs (vs. CCl 4 ‐activated mHSCs). Of the 35 genes that were uniquely up‐regulated in alcohol‐activated hHSCs/mHSCs, CSF1R , PLEK , LAPTM5 , CD74 , CD53 , MMP9 , CD14 , CTSS , TYROBP , and ITGB2 were identified as signature genes of alcohol‐activated hHSCs/mHSCs, and their functions were linked to fibrogenic/ECM‐associated pathways and immuno‐regulatory pathways in myofibroblasts . By studying these pathways, we can target genes downstream of potential HSC activators and inhibit the response to injury.…”

Section: Discussionmentioning

confidence: 99%

“…Of the 35 genes that were uniquely up-regulated in alcohol-activated hHSCs/ mHSCs, CSF1R, PLEK, LAPTM5, CD74, CD53, MMP9, CD14, CTSS, TYROBP, and ITGB2 were identified as signature genes of alcohol-activated hHSCs/mHSCs, and their functions were linked to fibrogenic/ECM-associated pathways and immunoregulatory pathways in myofibroblasts. (27)(28)(29) By studying these pathways, we can target genes downstream of potential HSC activators and inhibit the response to injury. The ECM is a component of all mammalian tissues, consisting of the proteins collagen, elastin, and fibronectin.…”

Section: Discussionmentioning

confidence: 99%

Primary Alcohol‐Activated Human and Mouse Hepatic Stellate Cells Share Similarities in Gene‐Expression Profiles

et al. 2020

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Alcoholic liver disease (ALD) is a leading cause of cirrhosis in the United States, which is characterized by extensive deposition of extracellular matrix proteins and formation of a fibrous scar. Hepatic stellate cells (HSCs) are the major source of collagen type 1 producing myofibroblasts in ALD fibrosis. However, the mechanism of alcohol‐induced activation of human and mouse HSCs is not fully understood. We compared the gene‐expression profiles of primary cultured human HSCs (hHSCs) isolated from patients with ALD (n = 3) or without underlying liver disease (n = 4) using RNA‐sequencing analysis. Furthermore, the gene‐expression profile of ALD hHSCs was compared with that of alcohol‐activated mHSCs (isolated from intragastric alcohol‐fed mice) or CCl4‐activated mouse HSCs (mHSCs). Comparative transcriptome analysis revealed that ALD hHSCs, in addition to alcohol‐activated and CCl4‐activated mHSCs, share the expression of common HSC activation (Col1a1 [collagen type I alpha 1 chain], Acta1 [actin alpha 1, skeletal muscle], PAI1 [plasminogen activator inhibitor‐1], TIMP1 [tissue inhibitor of metalloproteinase 1], and LOXL2 [lysyl oxidase homolog 2]), indicating that a common mechanism underlies the activation of human and mouse HSCs. Furthermore, alcohol‐activated mHSCs most closely recapitulate the gene‐expression profile of ALD hHSCs. We identified the genes that are similarly and uniquely up‐regulated in primary cultured alcohol‐activated hHSCs and freshly isolated mHSCs, which include CSF1R (macrophage colony‐stimulating factor 1 receptor), PLEK (pleckstrin), LAPTM5 (lysosmal‐associated transmembrane protein 5), CD74 (class I transactivator, the invariant chain), CD53, MMP9 (matrix metallopeptidase 9), CD14, CTSS (cathepsin S), TYROBP (TYRO protein tyrosine kinase‐binding protein), and ITGB2 (integrin beta‐2), and other genes (compared with CCl4‐activated mHSCs). Conclusion: We identified genes in alcohol‐activated mHSCs from intragastric alcohol‐fed mice that are largely consistent with the gene‐expression profile of primary cultured hHSCs from patients with ALD. These genes are unique to alcohol‐induced HSC activation in two species, and therefore may become targets or readout for antifibrotic therapy in experimental models of ALD.

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Identification of differentially expressed genes regulated by molecular signature in breast cancer-associated fibroblasts by bioinformatics analysis

Cited by 8 publications

References 136 publications

Prediagnostic circulating inflammation biomarkers and esophageal squamous cell carcinoma: A case–cohort study in Japan

Prediagnostic circulating inflammation biomarkers and esophageal squamous cell carcinoma: A case–cohort study in Japan

Key genes affecting the progression of nasopharyngeal carcinoma identified by RNA-sequencing and bioinformatic analysis

Primary Alcohol‐Activated Human and Mouse Hepatic Stellate Cells Share Similarities in Gene‐Expression Profiles

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