The role of vimentin in regulating genes related to EMT
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE17802 | GEO | 2010/11/18
SECONDARY ACCESSION(S): PRJNA118337
REPOSITORIES: GEO
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Project description:To study the biological and functional role of vimentin in maintenance of the mesenchymal phenotype of mammary epithelial cells, vimentin was silenced in the non-transformed MCF10A cells and vimentin-dependent changes in gene expression were analyzed. Scrambled is the siScr-transfected control with two replicates; KD the sample with vimentin knockdown, also two replicates.
2010-11-18 | E-GEOD-17802 | biostudies-arrayexpress
Project description:To study the biological and functional role of vimentin in maintenance of the mesenchymal phenotype of mammary epithelial cells, vimentin was silenced in the non-transformed MCF10A cells and vimentin-dependent changes in gene expression were analyzed. Scrambled is the siScr-transfected control with two replicates; KD the sample with vimentin knockdown, also two replicates.
| S-ECPF-GEOD-17802 | biostudies-other
Project description:Primary mammary gland basal epithelial cells from adult vimentin knockout mice and their littermate controls
2017-10-11 | GSE104762 | GEO
Project description:Epithelial vimentin plays a functional role in mammary gland development
| PRJNA413784 | ENA
Project description:Vimentin is a Type III intermediate filament (VIF) cytoskeletal protein that regulates the mechanical and migratory behavior of cells. Its expression is considered to be a marker for the epithelial to mesenchymal transition (EMT) that takes place in tumor metastasis. However, the molecular mechanisms regulated by the expression of vimentin in the EMT remain largely unexplored. We created MCF7 epithelial cell lines expressing vimentin from a cumate-inducible promoter to address this question. When vimentin expression was induced in these cells, extensive cytoplasmic VIF networks were assembled accompanied by changes in the organization of the endogenous keratin intermediate filament (KIF) networks and disruption of desmosomes. Significant reductions in intercellular forces by the cells expressing VIFs were measured by quantitative monolayer traction force and stress microscopy. In contrast, laser trapping micro-rheology revealed that the cytoplasm of MCF7 cells expressing VIFs was stiffer than the uninduced cells. Vimentin expression activated transcription of genes involved in pathways responsible for cell migration and locomotion. Importantly, the EMT related transcription factor TWIST1 was upregulated only in WT vimentin expressing cells and not in cells expressing a mutant non-polymerized form of vimentin, which only formed unit length filaments (ULF). Taken together, our results suggest that vimentin expression induces a hybrid EMT correlated with the upregulation of genes involved in cell migration.
2022-09-30 | GSE206724 | GEO
Project description:The intermediate filament vimentin is present in immune cells. It provides structural support to cells and functions in macrophages to coordinate inflammatory responses. Neutrophils are an abundance innate immune cell that function by distinct mechanisms from macrophages to mediate antimicrobial activities. The role of vimentin in neutrophils is not established. Here, we developed an immortalized neutrophil model to examine the requirement of vimentin. We demonstrate that vimentin restricts proinflammatory cytokine production and reactive oxygen species production, but enhances phagocytosis and swarming. We observe that vimentin is dispensable for neutrophil extracellular trap (NET) formation, degranulation, and for inflammasome activation. Moreover, gene expression analysis defined vimentin presence was associated with expression changes in multiple genes required for mitochondrial function and ROS overproduction in the absence of vimentin. By treatment of cells producing vimentin with rotenone, an inhibitor for complex I of the electron transport chain, or by treatment of cells lacking vimentin with mitoTEMPO, a SOD mimetic, we complement the changes in ROS levels through manipulation of mitochondrial function. Together, we suggest vimentin regulates neutrophil antimicrobial functions and alters ROS levels through regulation of mitochondrial activity.
2024-09-12 | GSE262717 | GEO
Project description:Purpose:The Vimentin gene plays a pivotal role in epithelial-to-mesenchymal transition (EMT) and is known to be over-expressed in the prognostically poor basal-like breast cancer subtype. Recent studies have reported Vimentin DNA methylation in association with poor clinical outcomes in other solid tumors, but not in breast cancer. We therefore quantified Vimentin DNA methylation in breast tumors and matched normal pairs in association with gene expression and survival in a cohort of 83 breast cancer patients. Materials and Methods:Vimentin methylation was quantified in 14 breast cell lines, 83 breast tumors, and 57 matched normal pairs using MALDI-TOF mass spectrometry. Gene expression data via qRT-PCR in cell lines, and oligo microarray data from breast tissues was correlated with percent methylation in the Vimentin promoter. A threshold of 20 percent average methylation was set for bivariate and multivariate tests of association between methylation and tumor subtype, tumor histopathology, and survival. Results:Vimentin was differentially methylated in luminal breast cancer cell lines, and in luminal A, luminal B and HER2+ breast tumor subtypes, but was rare in basal-like cell lines and tumors. Increased methylation was strongly correlated with decreased mRNA expression in cell lines, and had a moderate inverse correlation in breast tumors. Importantly, Vimentin methylation predicted poor overall survival independent of race, subtype, stage, nodal status or estrogen receptor positivity. Conclusion:Vimentin methylation predicts overall survival in breast cancer patients and holds promise as a prognostic biomarker for guiding treatment and prophylaxis. reference x sample
2013-02-19 | E-GEOD-35629 | biostudies-arrayexpress
Project description:Purpose:The Vimentin gene plays a pivotal role in epithelial-to-mesenchymal transition (EMT) and is known to be over-expressed in the prognostically poor basal-like breast cancer subtype. Recent studies have reported Vimentin DNA methylation in association with poor clinical outcomes in other solid tumors, but not in breast cancer. We therefore quantified Vimentin DNA methylation in breast tumors and matched normal pairs in association with gene expression and survival in a cohort of 83 breast cancer patients. Materials and Methods:Vimentin methylation was quantified in 14 breast cell lines, 83 breast tumors, and 57 matched normal pairs using MALDI-TOF mass spectrometry. Gene expression data via qRT-PCR in cell lines, and oligo microarray data from breast tissues was correlated with percent methylation in the Vimentin promoter. A threshold of 20 percent average methylation was set for bivariate and multivariate tests of association between methylation and tumor subtype, tumor histopathology, and survival. Results:Vimentin was differentially methylated in luminal breast cancer cell lines, and in luminal A, luminal B and HER2+ breast tumor subtypes, but was rare in basal-like cell lines and tumors. Increased methylation was strongly correlated with decreased mRNA expression in cell lines, and had a moderate inverse correlation in breast tumors. Importantly, Vimentin methylation predicted poor overall survival independent of race, subtype, stage, nodal status or estrogen receptor positivity. Conclusion:Vimentin methylation predicts overall survival in breast cancer patients and holds promise as a prognostic biomarker for guiding treatment and prophylaxis.
2013-02-19 | GSE35629 | GEO
Project description:This study was designed to follow the transcriptome changes during BMP2 mediated transformation of the MCF10A human mammary stem cell model. We found that long-term BMP2/IL6 exposure of MCF10A cells, human immortalized but non-transformed mammary stem cells and progenitors, led to their luminal transformation. MC26 cells correspond to MCF10A cells transformed by BMP2/IL6 long-term exposure and contrarily to their parental cells, are able to engraft in immunodeficient mice and form colonies in soft-agar. M1B26 cells were obtained after BMP2/IL-6 long-term treatment of MCF10A cells sorted for high BMPR1B expression and subsequent isolation and expansion of 3 soft-agar colonies. M1B26 have an increased ability to engraft in mice and form colonies in soft-agar when compared to MC26 cells. As a non-transformed control, MCF10A-CT cells were kept in culture without BMP2/IL6 for the same length of time than MC26 cells. MCF10A-CT, MC26 and M1B26 cells are thus a model allowing to follow the molecular events associated with the initiation of a luminal transformation in mammary stem cells. Expression of the CD10 membrane endopeptidase has been associated with cancer although it can be a marker of both good or poor prognosis depending on the stage of the cancer and on the tissue of origin. In addition, we showed that CD10 was a marker of stem cell containing populations in healthy mammary tissue and that CD10 enzymatic activity was involved in the maintenance of cells immature properties. Having recently shown that CD10 expression was increasing during BMP2 mediated transformation and that CD10 expressing cells were more transformed but that CD10 was not required for transformation, we set out to determine the gene signature associated with CD10 expression.
2023-09-01 | GSE123053 | GEO
Project description:PHF8 exerts distinct functions in different types of cancer. However, the mechanisms underlying its specific functions in each case remain obscure. To establish whether overexpression of PHF8 regulates the TGF-β induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-β1 for 0, 24, 48 and 72 hours and performed RNA-seq in biological duplicates. Our data indicated that EMT gene signatures were significantly enriched in MCF10A-PHF8 cells with TGF-β1 treatment at all time points, strongly indicating that PHF8 overexpression induces a sustained EMT signaling program. mRNA profiles of MCF10A-Mock (control) and MCF10A-PHF8 with TGF-β1 treatment for 0, 24, 48 and 72 hours were generated by RNA-seq, in duplicate, using HiSeq2500 instrument.
2016-10-26 | E-GEOD-74377 | biostudies-arrayexpress