Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-16873
PROVIDER: PRJNA117579 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Early Dysregulation of Cell Adhesion and Extracellular Matrix Pathways in Breast Cancer Progression
2025-01-24 | E-GEOD-16873 | ExpressionAtlas
Project description:Deep proteomic profiling of luminal breast cancer progression
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Project description:The long-non-coding MALINC1 intergenic RNA (also known as LINC001024) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the MALINC1 expression and localization, their phenotypic and molecular effects in non-invasive and invasive breast cancer models. We determined that MALINC1 is a E2-ER modulated lncRNA enriched in the cytoplasmic fraction of luminal A/B breast cancer cells that is associated with worse overall survival in patients with primary invasive breast carcinomas (p=0.027). Transcriptomic studies (RNA-seq) in normal and DCIS cells identified the main signaling pathways modulated by MALINC1 which include bioprocesses related to extracellular matrix remodeling, epithelial cell migration, adhesion, proliferation, and activation of AP1 signaling pathway. We conclude that MALINC1 over-expression behaves as an oncogenic lncRNA both in normal and DCIS breast cells involved with early-stage breast cancer progression.
2022-06-30 | GSE194150 | GEO
Project description:The long-non-coding HOX transcript antisense intergenic RNA (HOTAIR) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the phenotypic effects and signaling pathways modulated by HOTAIR in early-stage breast cancer progression. We determined that HOTAIR induces premalignant phenotypic changes by increasing cell proliferation, migration, invasion and in vivo growth in normal and DCIS breast cell lines. Transcriptomic studies (RNA-seq) identified the main signaling pathways modulated by HOTAIR which include bioprocesses related to cell migration, epithelial to mesenchymal transition, extracellular matrix remodeling and activation of HIF1A, AP1 and FGFR signaling pathways among others. Similar pathways were identified as activated in primary invasive breast carcinomas with HOTAIR over-expression. We conclude that HOTAIR over-expression behaves as a positive regulator of cell growth and migration both in normal and DCIS breast cells involved with early-stage breast cancer progression.
2021-11-01 | GSE183058 | GEO
Project description:Breast cancer cell lines - palmitate vs control
2025-01-23 | E-MTAB-2601 | ExpressionAtlas
Project description:Tissue stiffness is a critical prognostic factor in breast cancer and is associated with metastatic progression. Here we show an alternative and complementary hypothesis of tumor progression whereby physiological matrix stiffness affects the quantity and protein cargo of small EVs produced by cancer cells, which in turn aid cancer cell dissemination. Primary patient breast tissue produces significantly more EVs from stiff tumor tissue than soft tumor adjacent tissue. EVs released by cancer cells on matrices that model human breast tumors (25 kPa; stiff EVs) feature increased adhesion molecule presentation (ITGα2β1, ITGα6β4, ITGα6β1, CD44) compared to EVs from softer normal tissue (0.5 kPa; soft EVs), which facilitates their binding to extracellular matrix (ECM) protein collagen IV, and a 3-fold increase in homing ability to distant organs in mice. In a zebrafish xenograft model, stiff EVs aid cancer cell dissemination. Moreover, normal, resident lung fibroblasts treated with stiff and soft EVs change their gene expression profiles to adopt a cancer associated fibroblast (CAF) phenotype. These findings show that EV quantity, cargo, and function depend heavily on the mechanical properties of the extracellular microenvironment.
2024-06-22 | PXD049019 | Pride
Project description:This model builds upon two published models focused on the early steps of metastasis by Cohen et al. and on EMT process by Selvaggio et. al. The initial model of Cohen and colleagues was built with two inputs: the ECMenv, which monitored the status of the extracellular matrix, and DNA_damage, which considered DNA alterations that trigger death signals. Four additional inputs were added to account for the presence of Oxygen, growth factors (as GF), TGFbeta and the contact with other neighboring cells (as Neigh). The phenotypes, or outputs of the model include CellCycleArrest, Apoptosis, EMT, ECM_adh (for cell adhesion), ECM_degrad (for cell degradation), Cell_growth (for the dynamics of the tumor growth) and Cell_freeze (for cell motility ability). New genes and pathways include mechanisms around p63 and SRC. Genes from the Hippo pathway and RhoGTPases, such as YAP1, FAK and RAC1 were also inserted to link external signals (i.e., cell–cell contact, stiffness of the extracellular matrix, and stress signals) and intracellular regulation. The resulting network encompasses 45 nodes, with 6 input nodes, representing the possible interactions of an individual cell with external elements, and 8 output nodes or read-outs describing the possible observed phenotypes.
This model was initially developed as a MaBoSS model for a multi-scale model of tumor invasion, developed with PhysiBoSS. As SBML-qual cannot describe fully a MaBoSS model yet, we also include the MaBoSS BND and CFG files.
2023-06-27 | MODEL2304070002 | BioModels
Project description:HOTAIR Modulated Pathways in Early-Stage Breast Cancer Progression
| PRJNA758976 | ENA
Project description:Parvin-beta is a focal adhesion protein downregulated in human breast cancer cells. Loss of Parvin-beta contributes to increased integrin-linked kinase activity, cell-matrix adhesion, and invasion through the extracellular matrix in vitro. The effect of ectopic Parvin-beta expression on the transcriptional profile of MDA-MB-231 breast cancer cells, which normally do not express Parvin-beta was evaluated. Particular emphasis was placed upon propagating MDA-MB-231 breast cancer cells in three-dimensional culture matrices. Gene expression profiles of vector control and Parvin-beta transfected MDA-MB-231 cells cultured on (A) monomeric type I collagen coated plastic, (B) embedded in a type I collagen gel, and (C) embedded in basement membrane (growth factor reduced Matrigel), were compared. Interestingly, Parvin-beta re-expression in MDA-MB-231 cells increased the mRNA expression, serine 82 phosphorylation (mediated by CDK9), and activity of the nuclear hormone receptor, peroxisome proliferator-activated receptor gamma (PPARgamma) and a concomitant increase in lipogenic gene expression as a downstream effector of PPARgamma. Importantly, Parvin-beta suppressed breast cancer growth in vivo with associated decreased proliferation. These data suggest that Parvin-beta might influence breast cancer progression.. Keywords: Gene expression profiling in two dimensional vs three dimensional cell culture
2007-12-14 | GSE9747 | GEO
Project description:MASTL (Microtubule associated serine-threonine kinase-like) is a relatively recently identified mitotic accelerator. There are also indications of its role in cancer progression, especially in breast cancer, but the molecular mechanisms behind this and the cell cycle independent functions of MASTL are poorly understood. Regulation of cell adhesion and actin dynamics play a central role in governing cell contractility, migration and cell division in normal and cancer cells. Here, we identify MASTL as regulator of cell contractility and activator of the transcriptional co-activator MTRF-A. We show that depletion of MASTL increases cell contact with the extracellular matrix, reduces contractile actin stress fibers in normal and breast cancer cells. Importantly, depletion of MASTL also leads to strongly impairs motility of breast cancer cells. Our transcriptome and proteome profiling revealed that depletion of MASTL impairs transcription and expression of several MRTF-A target genes implicated in cellular movement and actomyosin contraction, including Rho Guanine nucleotide exchange factor 2 (GEF-H1, ARHGEF2) and tropomyosin 4.2 (TPM4). Mechanistically, we find that MASTL is necessary for serum-induced activation of SRF/MTRF-A transcription and that exogenous expression of GEF-H1 in MASTL depleted cells is sufficient to restore cell contractility. Taken together, our results suggest that MASTL is a previously undescribed key regulator of cell morphology and the actin cytoskeleton through transcriptional control of multiple adhesion and actin cytoskeleton regulating genes with key roles in contractility, cell adhesion and migration. MASTL (Microtubule associated serine-threonine kinase-like) is a relatively recently identified mitotic accelerator. There are also indications of its role in cancer progression, especially in breast cancer, but the molecular mechanisms behind this and the cell cycle independent functions of MASTL are poorly understood. Regulation of cell adhesion and actin dynamics play a central role in cell migration, morphology and cancer progression, but the role of MASTL in these processes has not been evaluated. Here, we show that depletion of MASTL increases cell contact with the extracellular matrix in breast cancer cells. Importantly, depletion of MASTL also leads to reduction of contractile actin stress fibers and decreased cell motility. Further, our transcriptome and proteome profiling revealed that mechanistically depletion of MASTL impairs transcription and expression of regulators of cellular movement and actomyosin contraction, including Rho Guanine nucleotide exchange factor 2 (GEF-H1, ARHGEF2) and tropomyosin 4.2 (TPM4). Further, we show that the transcriptional changes are caused by defectiveness of the serum response factor (SRF) signalling. Importantly, this study reveals advanced role for MASTL in interphase cells that activates a transcriptional program strongly impacting on the expression of regulators of cellular motility and actomyosin contraction.
2020-04-14 | PXD013757 | Pride