Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MaTAR25 lncRNA regulates the Tensin1 gene to impact breast cancer progression

ABSTRACT: Misregulation of long non-coding RNA genes has been linked to a wide variety of cancer types. Here we report on Mammary Tumor Associated RNA 25 (MaTAR25), a nuclear enriched and chromatin associated lncRNA that plays a role in mammary tumor cell proliferation, migration, and invasion, both in vitro and in vivo. MaTAR25 functions by interacting with purine rich element binding protein B, and associating with a major downstream target gene Tensin 1 (Tns1) to regulate its expression in trans. Knockout of MaTAR25 results in down-regulation of Tns1 leading to a reorganization of the actin cytoskeleton, and a reduction of focal adhesions and microvilli. The human ortholog of MaTAR25, LINC01271, is upregulated with human breast cancer stage and metastasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE142169 | GEO | 2020/10/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Tensin 2 interactomics reveals interaction with GAPDH and a phosphorylation-mediated regulatory role in glycolysis

Project description:Integrin adaptor proteins, like tensin-2, are crucial for cell adhesion and signaling. However, the function of tensin-2 beyond localizing to focal adhesions remain poorly understood. We utilized proximity-dependent biotinylation and strep-tag affinity proteomics to identify interaction partners of tensin-2 in HEK293 cells. Interactomics linked tensin-2 to known focal adhesion proteins and the dystrophin glycoprotein complex, while also uncovering novel interaction with the glycolytic enzyme GAPDH. We demonstrated that Y483-phosphorylation of tensin-2 regulates the glycolytic rate in HEK293 and MEF cells and found that pY483 tensin-2 is enriched in adhesions in MEF cells. Our study unveils novel interaction partners for tensin-2 and further solidifies its speculated role in cell energy metabolism. These findings shed fresh insight on the functions of tensin-2, highlighting its potential as a therapeutic target for diseases associated with impaired cell adhesion and metabolism.

2024-07-20 | GSE231782 | GEO

Tensin 2 interactomics reveals interaction with GAPDH and a phosphorylation-mediated regulatory role in glycolysis

Project description:Integrin adaptor proteins, like tensin-2, are crucial for cell adhesion and signalling. However, its functions beyond localizing to focal adhesions remain poorly understood. To identify tensin-2's interaction partners in HEK293 cells, we utilized proximity-dependent biotinylation and strep-tag affinity proteomics. Results linked tensin-2 to known focal adhesion proteins and the dystrophin-glycoprotein complex, while also uncovering novel interaction with the glycolytic enzyme GAPDH. We demonstrated that Y483-phosphorylation of tensin-2 regulates the glycolytic rate in HEK293 and MEF cells, as well as gene expression in HEK293 cells. Of note, Y483-phosphorylation directs tensin-2 to adhesion sites in MEF cells. Our study unveils numerous novel interaction partners for tensin-2, further solidifies its speculated role in cell energy metabolism and identifies Y483-phosphorylation as a crucial regulator for tensin-2 localization. These findings shed fresh insight into the functions of tensin-2, highlighting its potential as a therapeutic target for diseases associated with impaired cell adhesion and metabolism.

2023-05-02 | MSV000091836 | MassIVE

Gene expression profiling of tumor cell lines with constitutively active STAT3

Project description:The transcription factor STAT3 is constitutively activated in tumors of different origin but the molecular bases for STAT3 addiction of tumor cells have not yet been clearly identified. We generated knock/in mice carrying the constitutively active Stat3 allele, Stat3C, and showed that Stat3C could enhance Neu oncogenic power, triggering the production of earlier onset, more invasive mammary tumors. Tumor-derived cell lines displayed higher migration and invasion and disrupted distribution of cell-cell junction markers. The tensin family member Cten (C-Terminal Tensin-like), known to mediate EGF-induced migration and highly expressed in inflammatory breast cancer, was up-regulated in both Neu;Stat3C cells and tumors. Both Cten expression and enhanced migration were strictly dependent on Stat3, and Cten silencing normalized cell migration and rescued cell-cell contact defects. Importantly, the pro-inflammatory cytokine IL-6 could mediate Cten induction in MCF10 cells, in an exquisitely Stat3-dependent way. This model allowed us to shed some light on the oncogenic role of Stat3 in the breast, suggesting moreover a mechanism through which inflammatory signals can cooperate with EGF receptors in inflammatory breast cancer.

2010-01-15 | GSE17182 | GEO

Stromal PTEN determines mammary epithelial response to radio-therapy

Project description:It is well-described that the tumor stroma participates in cancer progression, but whether stromal factors can initiate breast tumorigenesis remains unclear. Using our previously described stromal-specific phosphatase and tensin homolog (PTEN) deletion mouse model, we investigated transformative events in young, non-tumor bearing animals. Here, we show stromal PTEN deletion initiates radiation-induced genomic instability on neighboring mammary epithelium through paracrine epidermal growth factor receptor (EGFR) activation. In these mice, a single low dose of whole-body radiation induces mammary hyperplasia, a result that is prevented by pre-treatment with an EGFR inhibitor. We reveal that stromal PTEN is lost in a subset of normal breast samples and is predictive of recurrence in breast cancer patients. Combined, these data suggest both diagnostic and therapeutic chest wall radiotherapy may inadvertently predispose patients with focal stromal PTEN loss to secondary breast cancer, and that this predisposition may be treated prophylactically through EGFR inhibition.

2018-06-13 | GSE93784 | GEO

The Dictyostelium retinoblastoma-like rblA gene is a major regulator of S-phase, mitotic and developmental gene expression

Project description:In metazoans, the retinoblastoma tumor suppressor has two major functions. In the first, it represses genes whose products are required for S-phase entry and S-phase progression, and thus stabilizes the G1 phase. In a second function, Rb synergizes with factors that induce cell cycle exit and terminal differentiation. Using mRNAseq and microarray transcriptional profiling, we show that rblA, the Rb ortholog of the Amebozoan Dictyostelium, has both of these functions. We characterize the action of rblA in the Dictyostelium cell cycle in detail, and in particular show that it represses not only S-phase genes but also almost all genes whose products are involved in mitosis. We compare rblA null mutants with their parent strain Ax2 at two developmental stages, vegetative growth and the preculminant stage of fruiting body formation; cell cycle genes show misregulation in the mutant at both stages.

2011-11-02 | E-TABM-1087 | biostudies-arrayexpress

H3K27ac ChIP-seq BTIC vs. DGC

Project description:Brain tumor initiating cells (BTICs), also known as cancer stem cells, hijack high-affinity glucose uptake normally active in brain to maintain energy demands in dynamic tumor microenvironments. Using unbiased metabolomics and genomic analyses, we discovered that de novo purine synthesis is functionally upregulated in BTICs, mediating glucose-sustained anabolic metabolism. Inhibiting purine synthesis abrogated BTIC growth, self-renewal, and in vivo tumor formation by depleting intracellular pools of purine nucleotides, supporting purine synthesis as potential therapeutic point of fragility. In contrast, differentiated brain tumor cells retained proliferative potential with targeting of purine biosynthetic enzymes, suggesting a selective dependence in BTICs. Upstream transcriptional activation of purine synthesis is mediated by MYC. Elevated expression of purine synthetic enzymes correlates with poor prognosis in glioblastoma patients. Collectively, our results suggest that a stem-like state in brain cancer is associated with metabolic reprogramming to fuel tumor hierarchy, revealing potential BTIC cancer dependencies amenable to targeted therapy.

2017-03-20 | GSE95216 | GEO

In Situ Structure of Intestinal Apical Surface Reveals Nanovilli on Microvilli

Project description:Microvilli are actin bundle-supported membrane protrusions essential for absorption, secretion, and sensation. Microvilli defects cause human diseases, including gastrointestinal disorders and inherited deafness; however, mechanisms controlling microvilli formation and organization remain unclear. Here, we study microvilli by vitrifying the C. elegans larvae and mouse intestinal tissues with high-pressure freezing, thinning them by cryo-focused ion beam milling, cryo-electron tomography, and sub-tomogram averaging. We show that hundreds of previously unrecognized stick-like structures, which we refer to as nanovilli, decorate the lateral surface of C. elegans and mouse microvilli. The C. elegans 37.5-nm long and 4.5-nm wide nanovilli are composed of the protocadherin family protein CDH-8. Loss of nanovilli slows down animal growth and increases the number of Y-shaped microvilli, intermediate structures when a microvillus splits from its tip and separates into two. Our results indicate that nanovilli space microvilli and suggest a microvilli division model through which microvilli assemble with striking uniformity.

2021-04-30 | GSE167859 | GEO

Targeted Inhibition of Purine Metabolism is Effective in Suppressing Hepatocellular Carcinoma Progression

Project description:Tumor-specific metabolic rewiring, intended to confer a survival advantage over non-transformed cells, often offers an opportunity to target cancers. Here, we identify deregulated expression of purine biosynthetic enzymes as a metabolic hallmark in human hepatocellular carcinomas (HCC), with the extent of enzyme upregulation a predictor of clinical outcome. We demonstrate in HCC cell lines, patient-derived xenograft (PDX) organoids and mouse models that inhibition of purine biosynthesis abrogated cancer cell proliferation and tumor growth. Mechanistically, a PI3K-E2F1 axis coordinated purine biosynthetic enzyme expression. Clinically approved inhibitors against PI3K and the purine biosynthetic rate-limiting enzyme IMPDH synergistically reduced the tumor burden in a PDX mouse model. Collectively, our results support targeting purine metabolic reprogramming as a precision therapeutic strategy for HCC patients.

2020-07-06 | GSE145988 | GEO

Effect of TPA on focal adhesion composition

Project description:Effect of a tumor promoter TPA on collagen IV based focal adhesions from CHO cells expressing human integrin alpha1 with activating mutation E317A

2016-07-11 | PXD003153 | Pride

siRNA profiling of human SH-SY5Y cells after LSD1 knock down

Project description:To analyze the functional relevance of LSD1 in neuroblastic tumors, SH-SY5Y cells were transiently transfected with siRNA directed against LSD1 or with a scrambled control siRNA. Microarray analysis revealed changes in expression that were consistent with these observations 72 hours after LSD1 knock-down. At this time, 28 genes were significantly induced at least 1.5-fold and 29 genes were significantly repressed at least 1.5-fold. Among the 28 induced genes, 4 are markers of cytoskeletal remodelling (TNS1, TPM1, DNM2, DNAL4), indicating differentiation, and 3 (TPM1, DNM2 and SHANK2) are functionally linked to neurite dynamics and synaptic trafficking. TaqMan quantitative RT-PCR confirmed the expression changes detected via microarray analysis for LSD1, DNAL4, DNM2, TNS1 and TPM1 Experiment Overall Design: SH-SY5Y cells were transfected with siRNA directed against LSD1 or control siRNA. 2 independent transfection experiments were performed each. Reverse transcription, labelling of total RNA and subsequent hybridization to Affymetrix U133v2 chips were performed according to the manufacturerÂ´s protocols

2008-11-13 | E-GEOD-13273 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data