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Expression data from MCF-7 and MCF-7/ADR cells

ABSTRACT: Chemoresistance in breast cancer has been a great interest in past studies, however, the development of rational therapeutic strategies targeting chemoresistant cells is still a challenge for clinical oncology.The resistant property of MCF7/ADR cells was confirmed by long term culture with Dox, cell viability, and PARP cleavage assays. Microarray analysis was performed to compare the global differences of gene expression between MCF-7 and MCF-7/ADR cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76540 | GEO | 2016/01/05

SECONDARY ACCESSION(S): PRJNA307671

REPOSITORIES: GEO

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Expression data from MCF-7 and MCF-7/ADR cells

Project description:Chemoresistance in breast cancer has been a great interest in past studies, however, the development of rational therapeutic strategies targeting chemoresistant cells is still a challenge for clinical oncology.The resistant property of MCF7/ADR cells was confirmed by long term culture with Dox, cell viability, and PARP cleavage assays. Microarray analysis was performed to compare the global differences of gene expression between MCF-7 and MCF-7/ADR cells. MCF-7 and MCF-7/ADR gene expression profiles were analyzed. Total RNA were prepared for analysis with Affymetrix Human U133 Plus 2.0 arrays according to the manufacturerâs instructions.

2016-01-05 | E-GEOD-76540 | biostudies-arrayexpress

Caenorhabditis elegans strain:N2, adr-1, adr-2, adr-1;adr-2

Project description:Caenorhabditis elegans strain:N2, adr-1, adr-2, adr-1;adr-2 Transcriptome or Gene expression

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N‑Glycoproteomics Study of Putative N‑Glycoprotein Biomarkers of Drug Resistance in MCF‑7/ADR Cells

Project description:Currently, drug resistance of anti-cancer therapy has become the main cause of low survival rate and poor prognosis. Full understanding of drug resistance mechanisms is an urgent request for further development of anti-cancer therapy and improvement of prognosis. Here we present our N-glycoproteomics study of putative N-glycoprotein biomarkers of drug resistance in doxorubicin resistance breast cancer cell line michigan cancer foundation-7 (MCF-7/ADR) relative to parental michigan cancer foundation-7 (MCF-7) cells. Intact N-glycopeptides (IDs) from MCF-7/ADR and MCF-7 cells were enriched with zwitterionic hydrophilic interaction liquid chromatography (ZIC-HILIC), labeled with stable isotopic diethylation (SIDE), and analyzed with C18-RPLC-MS/MS (HCD with stepped normalized collision energies); these IDs were identifed with database search engine GPSeeker, and the diferentially expressed intact N-glycopeptides (DEGPs) were quantifed with GPSeekerQuan. With target-decoy searches and control of spectrum-level FDR≤1%, 322 intact N-glycopeptides were identifed; these intact N-glycopeptides come from the combination of 249 unique peptide backbones (corresponding to 234 intact N-glycoproteins) and 90 monosaccharide compositions (corresponding to 248 putative N-glycosites). The sequence structures of 165 IDs were confrmed with structure-diagnostic fragment ions. With the criteria of observation at least twice among the three technical replicates,≥1.5-fold change and p value<0.05, 20 DEGPs were quantifed, where fve of them were up-regulated and 15 of them were down-regulated; the corresponding intact N-glycoproteins as putative markers of drug resistance were discussed.

2023-12-30 | PXD036101 | Pride

Human Breast LC-MSMS - Quantitative site- and structure-specific N-glycoproteomics characterization of differential N-glycosylation in MCF-7/ADR cancer stem cells

Project description:Cancer stem cells (CSCs) are reported to be responsible for tumor initiation, progression, metastasis, and therapy resistance where P-glycoprotein (P-gp) as well as other glycoproteins are involved. Identification of these glycoprotein markers is critical for understanding the resistance mechanism and developing therapeutics. Here we report our comparative N-glycoproteomics study of MCF‐7/ADR vs. MCF-7 cells. With zic-HILIC enrichment, isotopic diethyl labeling, RPLC-MS/MS (HCD) analysis and GPSeeker DB search, differentially expressed N-glycosylation was quantitatively characterized at the intact N-glycopeptides levels.

2020-02-21 | PXD013836 | Pride

Genome-wide profiling of long noncoding RNA expression patterns in chemoresistant breast cancer cells

Project description:Long non-coding RNAs (lncRNAs) are involved in cancer progression. In this study, the lncRNA profiling were analyzed in chemoresistant and sensitive breast cancer cells. We found a group of dysregulated lncRNAs in chemoresistant cells. Expression of dysregulated lncRNAs are correlated with dysregulated mRNAs, and enriched in GO and KEGG pathways related with cancer progression and chemoresistance development. Within those lncRNA-mRNA interactions, some lncRNAs may cis-regulate neighboring protein coding genes and involved in chemoresistance. The lncRNA NONHSAT028712 was then validated to regulate nearby CDK2 and interfere with cell cycle and chemoresistance. Furthermore, we identified another group of lncRNAs trans-regulated gene expression via interacting with different transcription factors (TF). Whereby NONHSAT057282 and NONHSAG023333 was found to modulate chemoresistance and most likely interacted with ELF1 and E2F1 respectively. In conclusion, this study reported for the first time the lncRNA expression patterns in chemoresistant breast cancer cells, and provided a group of novel lncRNA targets in mediating chemoresistance development in both cis- and trans- action mode. MCF-7/ADM replication 3 times, MCF-7/WT replication 3 times

2016-05-28 | E-GEOD-81971 | biostudies-arrayexpress

O-GlcNAc sites identification and quantification proteomics analysis of O-GlcNAc chromatin in MCF-7 and MCF-7/ADR cells

Project description:We used a metabolic labeling (GalNAz) based O-GlcNAc sites identification and quantification proteomics method to compare the O-GlcNAc chromatin of MCF-7 and MCF-7/ADR cells. The O-GlcNAc chromatin-associated proteins can be metabolically labeled with azides, followed by reaction with a cleavable DADPS (dialkoxydiphenylsilane) alkyne-biotin linker and enrichment with streptavidin beads. After cleavage of DADPS by formic acid, O-GlcNAc modified peptides were quantitative analysis using tandem mass spectroscopy (MS).

2020-12-01 | PXD022857 | iProX

Upregulated mRNAs and lncRNAs in chemoresistant breast cancer

Project description:Chemoresistance is a major cause of poor prognosis of breast cancer.More and more mRNAs and lncRNAs are reported to upregulate chemoresistance in breast cancer.To explore the how mRNAs and lncRNAs involved in chemoresistance of breast cancer,we sceened upregulated mRNAs and lncRNA from parental MCF-7 , chemoresistant MCF-7 cells as well as 4 breast cancer tissue sensitive to chemotherapy and 4 resistant to chemotherapy . Total RNA was extracted using Trizol reagent. Agilent Human lncRNA Microarray V6 (4*180K) was used to analyze the global profiling of human lncRNAs and protein-coding transcripts in these samples. The microarray contains 83,835 lncRNAs and 27,233 coding genes.

2020-02-25 | E-MTAB-8787 | biostudies-arrayexpress

Putative N-glycoprotein markers of MCF-7/ADR cancer stem cells from N-glycoproteomics characterization of the whole cell lysate

Project description:Being the most malignant disease among females, breast cancer has morbidity and mortality in the first and second positions among various cancers [1]. Up to now, chemotherapy has been the most common therapy [2]; however, multidrug resistance (MDR) often occurs to give low overall survival rate. Thus, it is urgent to figure out the mechanism of chemotherapy resistance. The first step of drugs to attack tumor cells is to interact with the plasma membrane, and solute carrier (SLC) family proteins are uptake transporters [3]. On the other side, the efflux transporters (such as ATP-binding cassette, ABC) pump drug out of cancer cells [4]. The main mechanism of MDR is the upregulation of ATP-binding cassette (ABC) transporters [5]. Breast cancer resistance protein (ABCG2), multidrug resistance protein (ABCC1) and P-glycoprotein (P-gp) have been extensively studied [6,7]. Formation of CSCs [8], DNA damage [9] and cell apoptosis [10] and epithelial mesenchymal transition (EMT) are other mechanisms of MDR. To zoom in on the correlation between altered glycosylation and drug resistance and to find out the putative biomarkers, MS-based glycoprotomics is a method of choice. Here, we report our N-glycoproteomics study of differential N-glycosylation from the whole cell lysate of MCF-7/ADR CSCs (adriamycin-resistant MCF-7 CSCs) relative to MCF-7 CSCs. Intact N-glycopeptides from both cells were enriched with ZIC-HILIC, isotopically diethylated, mixed with 1:1 ratio, and the mixture was analyzed by C18-RPLC-ESI-MS/MS (HCD with stepped NCE). Differentially expressed N-glycopeptides (DEGPs) were identified and quantified with database search using GPSeeker.

2023-07-04 | PXD036095 | Pride

Chryseobacterium sp. ADR-1

Project description:Chryseobacterium sp. ADR-1 Genome sequencing

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AVA-ADR-001- a small molecular inhibitor of ADAR1 (Immuno-oncology target)

Project description:To inhibitors for ADAR1 and a strong rationale for the development of ADAR1 p150 inhibitors for cancer immunotherapy Here, we describe AVA-ADR-001, a potential first-in-class small molecule inhibitor of ADAR1 p150 targeting the Z alpha domain. AVA-ADR-001 binds specifically to the Z alpha domain of ADAR1 p150 as confirmed by fluorescence spectroscopy and showed significant interferon induction in THP1 macrophages, which have high ADAR1 p150 expression compared with monocytes. Proteomics and transcriptomics analysis revealed significant upregulation of interferon signaling upon treatment with AVA-ADR -001. Interestingly, activation of interferon signaling resulted in AVA-ADR-001 induced cell killing in ADAR1-independent cell lines. In addition, treatment with AVA-ADR -001 resulted in significant activation of PKR, which may explain the decreased cell proliferation. Finally, AVA-ADR-001 showed superior anti-tumor efficacy compared to anti-PD1 in an in vivo tumor efficacy study and has a moderately synergistic effect when combined. Overall, this study reveals that ADAR1 p150 inhibition by AVA-ADR-001 exerts a multipronged impact on anti-tumor efficacy mediated by immune cells, accumulation of interferons and activation of PKR, resulting in protein translation inhibition and cell proliferation arrest.

2023-04-17 | GSE229503 | GEO

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