scholarly journals Pan-cancer survey of epithelial-mesenchymal transition markers across the Cancer Genome Atlas

2017 ◽  
Vol 247 (3) ◽  
pp. 555-564 ◽  
Author(s):  
Don L. Gibbons ◽  
Chad J. Creighton
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Mesenchymal Transition ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

scholarly journals Down-Regulation of miR-194-5p for Predicting Metastasis in Breast Cancer Cells

2021 ◽  
Vol 23 (1) ◽  
pp. 325
Author(s):  
Yu-Ting Yen ◽  
Jou-Chun Yang ◽  
Jiun-Bo Chang ◽  
Shih-Chang Tsai
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Mesenchymal Transition ◽  
Clinical Specimens ◽  
Cancer Genome Atlas ◽  
Genome Atlas

MicroRNAs (miRNAs), as key negative regulators of gene expression, are closely related to tumor occurrence and progression. miR-194-5p (miR-194-1) has been shown to play a regulatory role in various cancers however, its biological function and mechanism of action in breast cancer have not yet been well explored. In this study, we use the UALCAN and LinkedOmics databases to analyze transcription expression in The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA). The epithelial-mesenchymal transition status of breast cancer cells was evaluated by wound-healing assay, trans-well assays, and gelatin zymography, while protein expression was assessed by Western blotting. miR-194-5p expression was found to be up-regulated in breast cancer clinical specimens but down-regulated in the triple-negative breast cancer (TNBC) cell line MDA-MB-231 and breast cancer clinical specimens in The Cancer Genome Atlas (TCGA). miR-194-5p significantly inhibited the expression of the epithelial marker ZO-1 and increased the expression of mesenchymal markers, including ZEB-1 and vimentin, in MDA-MB-231 cells. miR-194-5p significantly reduced the gelatin-degrading activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 in zymography assays. In MDA-MB-231 cells and TCGA patient samples, ZEB-1 expression was significantly inversely correlated with miR-194-5p expression. High levels of miR-194-5p were associated with good overall survival. miR-194-5p regulates epithelial–mesenchymal transition (EMT) in TNBC. Our findings suggest that miR-194-5p functions as a tumor biomarker in breast cancer, providing new insights for the study of breast cancer development and metastasis.

scholarly journals Molecular Correlates of Metastasis by Systematic Pan-Cancer Analysis Across The Cancer Genome Atlas

2018 ◽  
Vol 17 (2) ◽  
pp. 476-487 ◽  
Author(s):  
Fengju Chen ◽  
Yiqun Zhang ◽  
Sooryanarayana Varambally ◽  
Chad J. Creighton
Keyword(s):  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

scholarly journals PR/SET Domain Family and Cancer: Novel Insights from the Cancer Genome Atlas

2018 ◽  
Vol 19 (10) ◽  
pp. 3250 ◽  
Author(s):  
Anna Sorrentino ◽  
Antonio Federico ◽  
Monica Rienzo ◽  
Patrizia Gazzerro ◽  
Maurizio Bifulco ◽  
...  
Keyword(s):  
Family Members ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Driver Gene ◽  
Rna Seq ◽  
Set Domain ◽  
Primary Tumors ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

The PR/SET domain gene family (PRDM) encodes 19 different transcription factors that share a subtype of the SET domain [Su(var)3-9, enhancer-of-zeste and trithorax] known as the PRDF1-RIZ (PR) homology domain. This domain, with its potential methyltransferase activity, is followed by a variable number of zinc-finger motifs, which likely mediate protein–protein, protein–RNA, or protein–DNA interactions. Intriguingly, almost all PRDM family members express different isoforms, which likely play opposite roles in oncogenesis. Remarkably, several studies have described alterations in most of the family members in malignancies. Here, to obtain a pan-cancer overview of the genomic and transcriptomic alterations of PRDM genes, we reanalyzed the Exome- and RNA-Seq public datasets available at The Cancer Genome Atlas portal. Overall, PRDM2, PRDM3/MECOM, PRDM9, PRDM16 and ZFPM2/FOG2 were the most mutated genes with pan-cancer frequencies of protein-affecting mutations higher than 1%. Moreover, we observed heterogeneity in the mutation frequencies of these genes across tumors, with cancer types also reaching a value of about 20% of mutated samples for a specific PRDM gene. Of note, ZFPM1/FOG1 mutations occurred in 50% of adrenocortical carcinoma patients and were localized in a hotspot region. These findings, together with OncodriveCLUST results, suggest it could be putatively considered a cancer driver gene in this malignancy. Finally, transcriptome analysis from RNA-Seq data of paired samples revealed that transcription of PRDMs was significantly altered in several tumors. Specifically, PRDM12 and PRDM13 were largely overexpressed in many cancers whereas PRDM16 and ZFPM2/FOG2 were often downregulated. Some of these findings were also confirmed by real-time-PCR on primary tumors.

scholarly journals Erratum: Corrigendum: A pan-cancer proteomic perspective on The Cancer Genome Atlas

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Rehan Akbani ◽  
Patrick Kwok Shing Ng ◽  
Henrica M.J. Werner ◽  
Maria Shahmoradgoli ◽  
Fan Zhang ◽  
...  
Keyword(s):  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

scholarly journals FXR silencing in human colon cancer by DNA methylation and KRAS signaling

2014 ◽  
Vol 306 (1) ◽  
pp. G48-G58 ◽  
Author(s):  
Ann M. Bailey ◽  
Le Zhan ◽  
Dipen Maru ◽  
Imad Shureiqi ◽  
Curtis R. Pickering ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Colon Cancer ◽  
Epithelial To Mesenchymal Transition ◽  
Human Colon ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Human Colon Cancer ◽  
Mesenchymal Transition ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Farnesoid X receptor (FXR) is a bile acid nuclear receptor described through mouse knockout studies as a tumor suppressor for the development of colon adenocarcinomas. This study investigates the regulation of FXR in the development of human colon cancer. We used immunohistochemistry of FXR in normal tissue ( n = 238), polyps ( n = 32), and adenocarcinomas, staged I–IV ( n = 43, 39, 68, and 9), of the colon; RT-quantitative PCR, reverse-phase protein array, and Western blot analysis in 15 colon cancer cell lines; NR1H4 promoter methylation and mRNA expression in colon cancer samples from The Cancer Genome Atlas; DNA methyltransferase inhibition; methyl-DNA immunoprecipitation (MeDIP); bisulfite sequencing; and V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) knockdown assessment to investigate FXR regulation in colon cancer development. Immunohistochemistry and quantitative RT-PCR revealed that expression and function of FXR was reduced in precancerous lesions and silenced in a majority of stage I-IV tumors. FXR expression negatively correlated with phosphatidylinositol-4, 5-bisphosphate 3 kinase signaling and the epithelial-to-mesenchymal transition. The NR1H4 promoter is methylated in ∼12% colon cancer The Cancer Genome Atlas samples, and methylation patterns segregate with tumor subtypes. Inhibition of DNA methylation and KRAS silencing both increased FXR expression. FXR expression is decreased early in human colon cancer progression, and both DNA methylation and KRAS signaling may be contributing factors to FXR silencing. FXR potentially suppresses epithelial-to-mesenchymal transition and other oncogenic signaling cascades, and restoration of FXR activity, by blocking silencing mechanisms or increasing residual FXR activity, represents promising therapeutic options for the treatment of colon cancer.

scholarly journals The Biological Function Delineated Across Pan-Cancer Levels Through lncRNA-Based Prognostic Risk Assessment Factors for Pancreatic Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Xudong Tang ◽  
Mengyan Zhang ◽  
Liang Sun ◽  
Fengyan Xu ◽  
Xin Peng ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Prognostic Marker ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Research Network ◽  
Molecular Characteristics ◽  
Cancer Data ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

Long non-coding RNAs (lncRNAs) play key roles in tumors and function not only as important molecular markers for cancer prognosis, but also as molecular characteristics at the pan-cancer level. Because of the poor prognosis of pancreatic cancer, accurate assessment of prognosis is a key issue in the development of treatment plans for pancreatic cancer. Here we analyzed pancreatic cancer data from The Cancer Genome Atlas and The Genotype Tissue Expression database using Cox regression and lasso regression in analyses using a combination of the two databases as well as only The Cancer Genome Atlas database (Cancer Genome Atlas Research Network et al., 2013). A prognostic risk score model with significant correlation with pancreatic cancer survival was constructed, and two lncRNAs were investigated. Additional analysis of 33 cancers using the two lncRNAs showed that lncRNA TsPOAP1-AS1 was a prognostic marker of seven cancers, among which pancreatic cancer was the most significant, and lncRNA mi600hg was a prognostic marker of ovarian cancer and pancreatic cancer. LncRNA TsPOAP1-AS1 is associated with clinical stage and tumor mutation burden of some cancers as well as a strong degree of immune infiltration in many cancers, while a strong correlation between lncRNA mi600hg and microsatellite instability was observed in several cancers. The results of this study help further our understanding of the different functions of lncRNAs in cancer and may aid in the clinical application of lncRNAs as prognostic factors for cancer.

scholarly journals ITGA3 Is a Reliable Biomarker and Putative Therapeutic Target for Glioma

2020 ◽  
Author(s):  
Qing Zhang ◽  
Chen Zhu ◽  
Gefei Guan ◽  
Shuai Shen ◽  
Yunhe Han ◽  
...  
Keyword(s):  
Therapeutic Target ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Glioma Cells ◽  
The Cancer Genome Atlas ◽  
Integrin Subunit ◽  
Central Nervous System Tumor ◽  
Mesenchymal Transition ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Abstract Background: Glioma is the most prevalent and malignant primary central nervous system tumor in adults. As a member of the integrin alpha chain family of proteins, integrin subunit alpha 3 (ITGA3) has been found to play a critical role in the occurrence and progression of several cancers, including lung, ovarian, and pancreatic cancers. However, the role of ITGA3 in glioma remains unclear.Methods: The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), REMBRANDT, GSE16011, GSE59612, and GSE4290 datasets were used to analyze relevant characteristics of ITGA3 in glioma. R language and GraphPad Prism 7.00 were employed as major tools for statistical analysis and graph manipulation.Results: We identified that ITGA3 expression was upregulated in glioma and related to unfavorable outcomes of glioma patients. Expression of ITGA3 also tended to be enriched in aggressive subtypes of glioma. We demonstrated that expression of ITGA3 was negatively correlated with glioma purity. In gliomas with high ITGA3 expression, the anti-glioma immune response was inhibited. ITGA3 also regulated angiogenesis within the glioma microenvironment and promoted the epithelial–mesenchymal transition (EMT) and autophagy of glioma cells. GSEA analysis revealed that ITGA3 could activate ERK1/2 and PI3K/AKT/mTOR pathways.Conclusion: Our data suggested that ITGA3 promoted the malignant progression of glioma by regulating the immunity of glioma as well as the EMT and autophagy of glioma cells, which could act as a therapeutic target for glioma.

scholarly journals Aging-Related Tumor Microenvironment Changes Could Worsen The Prognosis of GBM Patients

2020 ◽  
Author(s):  
Hongwang Song ◽  
Xiaojun Fu ◽  
Chenxing Wu ◽  
Shouwei Li
Keyword(s):  
Tumor Microenvironment ◽  
Epithelial Mesenchymal Transition ◽  
Close Correlation ◽  
Underlying Mechanism ◽  
The Cancer Genome Atlas ◽  
Future Research ◽  
Mesenchymal Transition ◽  
Cancer Genome Atlas ◽  
Differential Expressed Genes ◽  
Genome Atlas

Abstract Background: Glioblastoma multiforme (GBM) is the most malignant tumor in human brain, with highly heterogeneity among different patients. Age could function as an incidence and prognosis risk factor for many tumors.Method: A series of bioinformatic experiments were conducted to evaluate the differences of incidence, differential expressed genes, enriched pathways with the data from Surveillance, Epidemiology, and End Results (SEER) program, the cancer genome atlas (TCGA) and Chinese glioma genome atlas (CGGA) project.Results: We discovered in our present study that distinct difference of incidence and prognosis of different aged GBM patients. By a series of bioinformatic method, we found that the tumor associated fibroblasts (TAFs) was the most crucial tumor microenvironment (TME) component that led to this phenomenon. Epithelial-mesenchymal transition (EMT) could be the mechanism by which TAFs regulate the progression of GBM. Conclusion: We have proposed a close correlation between age and GBM incidence and prognosis, and propose the underlying mechanism behind this correlation by mining different databases, which laid the foundation for future research.

scholarly journals The Cancer Genome Atlas Pan-Cancer analysis project

2013 ◽  
Vol 45 (10) ◽  
pp. 1113-1120 ◽  
Author(s):  
John N Weinstein ◽  
◽  
Eric A Collisson ◽  
Gordon B Mills ◽  
Kenna R Mills Shaw ◽  
...  
Keyword(s):  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Cancer Genome Atlas ◽  
Pan Cancer ◽  
Genome Atlas

scholarly journals Aging-related tumor associated fibroblasts changes could worsen the prognosis of GBM patients

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hongwang Song ◽  
Xiaojun Fu ◽  
Chenxing Wu ◽  
Shouwei Li
Keyword(s):  
Risk Factor ◽  
Epithelial Mesenchymal Transition ◽  
Close Correlation ◽  
Underlying Mechanism ◽  
The Cancer Genome Atlas ◽  
Future Research ◽  
Mesenchymal Transition ◽  
Cancer Genome Atlas ◽  
Differential Expressed Genes ◽  
Genome Atlas

Abstract Background Glioblastoma multiforme (GBM) is the most malignant tumor in human brain, with highly heterogeneity among different patients. Age could function as an incidence and prognosis risk factor for many tumors. Method A series of bioinformatic experiments were conducted to evaluate the differences of incidence, differential expressed genes, enriched pathways with the data from Surveillance, Epidemiology, and End Results (SEER) program, the cancer genome atlas (TCGA) and Chinese glioma genome atlas (CGGA) project. Results We discovered in our present study that distinct difference of incidence and prognosis of different aged GBM patients. By a series of bioinformatic method, we found that the tumor associated fibroblasts (TAFs) was the most crucial tumor microenvironment (TME) component that led to this phenomenon. Epithelial-mesenchymal transition (EMT) could be the mechanism by which TAFs regulate the progression of GBM. Conclusion We have proposed a close correlation between age and GBM incidence and prognosis, and propose the underlying mechanism behind this correlation by mining different databases, which laid the foundation for future research.

Sign in / Sign up

Export Citation Format

Share Document