Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human breast cancer cell line LC-MS/MS

ABSTRACT: Long non-coding RNAs (lncRNA) have been identified as key regulators of tumorigenesis and development. We aim to explore the biological functions and molecular mechanisms of lncRNA MIR200CHG in breast cancer. We found that MIR200CHG is highly expressed in breast cancer tissues and is related to the tumor size and histopathological grade. In vitro and in vivo experiments confirmed that MIR200CHG can promote breast cancer proliferation, invasion, and drug resistance. MIR200CHG directly binds to the transcription factor Y-box binding protein-1 (YB-1), and inhibits its ubiquitination and degradation. MIR200CHG regulates YB-1 phosphorylation at serine 102, thereby affecting the expression of genes related to tumor cell proliferation, apoptosis, invasion, and drug resistance. Additionally, MIR200CHG partially affects the expression of miR-200c/141-3p encoded by its intron region. Therefore, MIR200CHG can promote the proliferation, invasion, and drug resistance of breast cancer by interacting with and stabilizing YB-1, and has the potential to become a target for breast cancer treatment.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Breast Cancer

SUBMITTER: li tang

LAB HEAD: feng yan

PROVIDER: PXD026480 | Pride | 2022-05-27

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20181224_001_gel_CHG_anti.wiff	Wiff
	20181224_001_gel_CHG_sen.wiff	Wiff
	Supplementary_Data.xlsx	Xlsx

Items per page:

1 - 3 of 3

Similar Datasets

AC016745.3 RNA pulldown mass spectrometry data

Project description:In order to find the protein specifically bound by lncRNA-AC016745.3, we identified it through RNA pulldown combined with Protein Mass Spectrometry

2022-02-15 | PXD029141 | Pride

TUBA1C: a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression

Project description:Background: The lack of obvious symptoms of early gastric cancer (GC) as well as the absence of sensitive and specific biomarkers results in poor clinical outcomes. Tubulin is currently emerging as important regulators of the microtubule cytoskeleton and thus have a strong potential to be implicated in a number of disorders, however, its mechanism of action in gastric cancer is still unclear. Tubulin alpha-1C(TUBA1C) is a subtype of α-tubulin, high TUBA1C expression has been shown to be closely related to a poor prognosis in in various cancers,this study, for the first time, revealed the mechanism of TUBA1C promotes malignant progression of gastric cancer in vitro and in vivo. Methods: The expression of lncRNA EGFR-AS1 was detected in human GC cell lines by qRT–PCR. Mass spectrometry experiments following RNA pulldown assays found that EGFR-AS1 directly binds to TUBA1C, the CCK8, EdU, transwell, wound-healing, cell cycle assays and animal experiments were conducted to investigate the function of TUBA1C in GC. Combined with bioinformatics analyses, reveal interaction between Ki-67, E2F1, PCNA and TUBA1C by western blot. Rescue experiments furtherly demonstrated the relationship of EGFR-AS1and TUBA1C. Results: TUBA1C was proved to be a direct target of EGFR-AS1, TUBA1C promotes gastric cancer proliferation, migration and invasion by accelerating the progression of the cell cycle from the G1 phase to the S phase and activating the expression of oncogenes: Ki-67,E2F1 and PCNA. Conclusions: TUBA1C is a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression and could be a novel biomarker and therapeutic target for GC.

2023-05-10 | PXD040199 | Pride

Breast cancer cell MCF7+CYP1B1-AS1 LC-MS/MS

Project description:Long non-coding Rnas (lncRNAs) can act as oncogenes or tumor suppressors to regulate cancer development. We found that CYP1B1-AS1 was down-regulated in breast cancer tissues and correlated with the prognosis of patients. Lentiviral vectors were used to overexpress CYP1B1-AS1 in MCF7 cells, and the target proteins bound to CYP1B1-AS1 were detected by pulldown assay and mass spectrometry. The function of CYP1B1-AS1 is unknown. Our study revealed the molecular mechanism of CYP1B1-AS1 inhibiting breast cancer proliferation in breast cancer, and provided a new strategy for the treatment of breast cancer targeting lncRNA.

2023-10-24 | PXD037317 | Pride

LETR1 (LINC01197) RNA pull-down in human LECs followed by LC-MSMS

Project description:Recent studies have revealed the importance of long noncoding RNAs (lncRNAs) as tissue-specific regulators of gene expression. There is ample evidence that distinct types of vasculature undergo tight transcriptional control to preserve their structure, identity, and functions. We determined, for the first time, the global lineage-specific lncRNAome of human dermal blood and lymphatic endothelial cells (BECs and LECs), combining RNA-Seq and CAGE-Seq. A subsequent genome-wide antisense oligonucleotide-knockdown profiling of two BEC- and two LEC-specific lncRNAs identified LETR1 as a critical gatekeeper of the global LEC transcriptome. Deep RNA-DNA and RNA-protein interaction studies, and phenotype rescue analyses revealed that LETR1 is a nuclear trans-acting lncRNA modulating, via key epigenetic factors, the expression of essential target genes governing the growth and migratory ability of LECs. Together, our study provides new evidence supporting the intriguing concept that every cell type expresses precise lncRNA signatures to control lineage-specific regulatory programs.

2020-12-21 | PXD018578 | Pride

Expression data from HepG2 cells before and after RNF43 knockdown

Project description:It has been demonstrated that Ring finger protein 43 (RNF43) is overexpressed in colorectal cancer and mediates cancer cell proliferation. We found that RNF43 was frequently overexpressed in HCC, and knockdown of RNF43 could induce apoptosis and inhibit proliferation, invasion, colony formation and xenograft growth of HCC cells. Suggesting that RNF43 is involved in tumorigenesis and progression of HCC. We used microarrays to profile gene expression patterns before and after RNF43 knockdown, and identified differentially expressed genes during this process. HepG2 cells were transfected with RNF43 siRNA or negative control siRNA in triplicate. Forty-eight hours after transfection, total RNA was extracted,labeled and hybridized to HG-U133 Plus 2.0 arrays.

2012-10-04 | E-GEOD-41326 | biostudies-arrayexpress

Mechanism and transcriptional program of YB-1 in breast cancer cell lines.

Project description:YB-1 controls epithelial-mesenchymal transitions by restricting translation of growth-related mRNAs and enabling expression of EMT-inducing transcription factors. We used microarrays to characterize the direct transcriptional and indirect translational regulation of mRNAs by exogenous YB-1 in breast cancer cell lines. Keywords: gene expression profiling To evaluate this in a genome-wide manner we compared microarray expression profiles of total mRNA and mRNAs isolated from Ps (translationally active) or post-Ps (translationally inactive) fractions of MCF10AT-MSCV vs. MCF10AT-YB-1 cells

2008-10-30 | E-GEOD-13410 | biostudies-arrayexpress

Proteome analysis of binding protein of lncRNA Cpmer in mesoderm cells

Project description:These proteome datasets demonstrate the binding proteins of lncRNA Cpmer in mesoderm cells during mouse ESCs derived cardiomyocyte differentiation process. Antisense-Cpmer is used as negative conrol.

2022-04-08 | PXD031814 | Pride

Effects of YB-1 protein reduction on microRNA abundance in breast cancer cell-lines

Project description:To assess the association of the nucleic acid binding protein yb-1 with mature microRNAs levels in breast cancer. To do this we performed YB-1 siRNA treatement in triplicates alongside an siRNA control Two breast cancer cell-lines, representative of Luminal A and Basal molecular subtypes were used, MCF7 and MDA-MB-435S.

2014-01-23 | GSE50087 | GEO

Pooled genome-wide analysis to identify novel risk loci for pediatric allergic asthma

Project description:We performed a pooled GWAS and individual genotyping in 269 children with allergic respiratory diseases comparing allergic children with and without asthma. We used a modular approach to identify the most significant loci associated with asthma by combining silhouette statistics and physical distance method with cluster-adapted thresholding. We found 97% concordance between pooled GWAS and individual genotyping, with 36 out of 37 top-scoring SNPs significant at individual genotyping level. The most significant SNP is located inside the coding sequence of C5, an already identified asthma susceptibility gene, while the other loci regulate functions that are relevant to bronchial physiopathology, as immune- or inflammation-mediated mechanisms and airway smooth muscle contraction. Integration with gene expression data (from mouse experimental asthma model taken from GSE6858 and GSE1301) showed that almost half of the putative susceptibility genes are differentially expressed in experimental asthma mouse models. Affymetrix SNP arrays (Mapping 250K NspI and StyI) were performed according to the manufacturer's directions on pooled DNA extracted from peripheral blood samples.The design is a pooled-GWAS. DNA samples were assigned to the Asthma group if displaying symptoms of asthma, alone or associated to other allergic phenotypes, including rhinoconjunctivitis (RC), and assigned to the RC group if displaying rhinitis or rhinoconjunctivits alone or associated to other allergic phenotypes, excluding asthma. Each of the two groups was subdiveded into 4 independent groups of samples, each containing 31-36 individuals. Individual DNA samples were then added to their respective pools in equivalent molar amounts. Each pool was labeled and hybridized independently on three different arrays (3 technical replicates for each pool).

2011-03-17 | E-GEOD-24481 | biostudies-arrayexpress

LincK promotes proliferation and epithelial-to-mesenchymal transition and contributes to tumorigenesis and growth in breast cancer I

Project description:In this study, we aimed to identify potential lncRNA deregulations associated with breast cancer malignancy instigated by MSCs-MCF7 co-culture. We profiled expression changes of lncRNAs in MCF-7 cells during EMT induced by coculture with hAD-MSCs, and found an intergenic lncRNA with proviouly unknown function (KB-1732A1.1, we termed it LincK), which was significantly elevated. Depletion of LincK decreased the growth, migration, invasion, and EMT in breast cancer cells, while overexpression of LincK exerted the opposite effects. Moreover, knockdown of LincK repressed tumorigenesis, and ectopic expression of LincK promoted tumor growth in MCF-7 xenograft model. LincKs can act as a sponge of mirR-200b, which inhibits its function in proliferation and metastasis. Thus we reported, for the ﬁrst time, the role of LincK in control of EMT and proliferation in breast cancer. We used microarrays to detail the genes associated with LincK.

2019-01-09 | GSE109007 | GEO