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EMT is the dominant program in human colon cancer (lung)

ABSTRACT: mRNA profiling of 93 lung cancer cell lines supporting data for PMID: 21251323 93 lung cancer cell lines profiled at baseline

ORGANISM(S): Homo sapiens

SUBMITTER: Loboda A

PROVIDER: S-ECPF-GEOD-28709 | biostudies-other | 2011

REPOSITORIES: biostudies-other

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EMT is the dominant program in human colon cancer.

Project description:BackgroundColon cancer has been classically described by clinicopathologic features that permit the prediction of outcome only after surgical resection and staging.MethodsWe performed an unsupervised analysis of microarray data from 326 colon cancers to identify the first principal component (PC1) of the most variable set of genes. PC1 deciphered two primary, intrinsic molecular subtypes of colon cancer that predicted disease progression and recurrence.ResultsHere we report that the most dominant pattern of intrinsic gene expression in colon cancer (PC1) was tightly correlated (Pearson R = 0.92, P < 10(-135)) with the EMT signature-- both in gene identity and directionality. In a global micro-RNA screen, we further identified the most anti-correlated microRNA with PC1 as MiR200, known to regulate EMT.ConclusionsThese data demonstrate that the biology underpinning the native, molecular classification of human colon cancer--previously thought to be highly heterogeneous-- was clarified through the lens of comprehensive transcriptome analysis.

| S-EPMC3032646 | biostudies-literature

EMT is the dominant program in human colon cancer (lung)

Project description:mRNA profiling of 93 lung cancer cell lines supporting data for PMID: 21251323 93 lung cancer cell lines profiled at baseline

2011-04-25 | E-GEOD-28709 | biostudies-arrayexpress

EMT is the dominant program in human colon cancer (lung)

Project description:mRNA profiling of 93 lung cancer cell lines supporting data for PMID: 21251323

2011-04-25 | GSE28709 | GEO

EMT is the dominant program in human colon cancer

Project description:This SuperSeries is composed of the following subset Series: GSE28567: EMT is the dominant program in human colon cancer (Affymetrix) GSE28709: EMT is the dominant program in human colon cancer (lung) GSE28722: EMT is the dominant program in human colon cancer (Agilent) Refer to individual Series

2011-04-25 | E-GEOD-28814 | biostudies-arrayexpress

EMT is the dominant program in human colon cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2011-04-25 | GSE28814 | GEO

EMT is the dominant program in human colon cancer (Affymetrix)

Project description:mRNA profiling data for 67 colorectal cancer at baseline Supporting data for PMID: 21251323 mRNA profiles at baseline for 67 colorectal cancer cell lines

2011-04-25 | E-GEOD-28567 | biostudies-arrayexpress

EMT is the dominant program in human colon cancer (Agilent)

Project description:mRNA profiles on 129 colorectal tumors 129 colorectal tumors profiled on Agilent array using pool of individual tumors as common reference

2011-04-25 | E-GEOD-28722 | biostudies-arrayexpress

EMT is the dominant program in human colon cancer (Agilent)

Project description:mRNA profiles on 129 colorectal tumors

2011-04-25 | GSE28722 | GEO

EMT is the dominant program in human colon cancer (Affymetrix)

Project description:mRNA profiling data for 67 colorectal cancer at baseline Supporting data for PMID: 21251323

2011-04-25 | GSE28567 | GEO

PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer.

Project description:The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molecular mechanisms and signaling cascades are entirely unknown. Here, we show that PRMT5 is the ectopic expression in human lung cancer tissues and cell lines. Further study reveals that silencing PRMT5 by lentivirus-mediated shRNA or blocking of PRMT5 by specific inhibitor GSK591 attenuates the expression levels of EMT-related markers in vivo, using the xenograft mouse model. Moreover, our results show that down-regulation of PRMT5 impairs EGFR/Akt signaling cascades in human lung cancer cells, whereas re-expression of PRMT5 recovers those changes, suggesting that PRMT5 regulates EMT probably through EGFR/Akt signaling axis. Altogether, our results demonstrate that PRMT5 serves as a critical oncogenic regulator and promotes EMT in human lung cancer cells. More importantly, our findings also suggest that PRMT5 may be a potential therapeutic candidate for the treatment of human lung cancer.

| S-EPMC8040599 | biostudies-literature

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