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Desmocollin-1 is associated with pro-metastatic phenotype of luminal A breast cancer cells and is modulated by parthenolide

ABSTRACT: Desmocollin-1 (DSC1) is a desmosomal transmembrane glycoprotein that maintains cell-to-cell adhesion. DSC1 was previously associated with lymph node metastasis of luminal A breast tumors and was found to increase metastatic potential of MCF7 cells in vitro. Therefore, we focused on DSC1 role in cellular and molecular mechanisms in luminal A breast cancer and its possible therapeutic modulation using parthenolide. We performed comparative gene expression analysis using data obtained from RNA-seq of DSC1-overexpressing and control cells treated and untreated with parthenolide in biological duplicates.

ORGANISM(S): Homo sapiens

PROVIDER: GSE228017 | GEO | 2023/09/06

REPOSITORIES: GEO

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Desmocollin-1 is associated with pro-metastatic phenotype of luminal A breast cancer cells and is modulated by parthenolide

Project description:Desmocollin-1 (DSC1) is a desmosomal transmembrane glycoprotein that maintains cell-to-cell adhesion. DSC1 was previously associated with lymph node metastasis of luminal A breast tumors and was found to increase metastatic potential of MCF7 cells in vitro. To delineate DSC1 role in breast cancer metastasis and evaluate possibilities of DSC1 modulation, we investigated the effect of DSC1 overexpression on morphology, cell survival, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying DSC1 gene (MCF7-DSC1-GFP). We moreover identified inhibitor parthenolide to decrease DSC1 protein levels and to modulate the molecular mechanisms associated with DSC1 in MCF7 cells. This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating DSC1 overexpression and parthenolide treatment in MCF7 breast cancer cell line, and results of pulldown analysis of DSC1-interacting proteins in MCF7 cells with and without parthenolide treatment.

2023-10-24 | PXD041029 | Pride

N-Linked Glycoprotein Profiles of Human Breast Luminal Malignant Cell Lines

Project description:Secreted proteins and transmembrane proteins with extracellular domains are frequently glycosylated; this group of proteins includes those that participate in the various intercellular junctions and signaling pathways of an epithelium. In this study we characterized the differences in glycoprotein expression between claudin-low and other breast cell lines using a dataset of 26 breast cell lines in which the glycoproteins were identified and quantitated by liquid chromatography/ tandem mass spectrometry. Our goals are to characterize the glycoproteome of a set of claudin-low lines, compare them to basal, luminal and non-malignant cells and to identify drugs that may be especially effective on these cell lines. These seven luminal malignant breast cells (BT474, HCC1428, MCF7, SKBR3, SUM185PE, T47D and ZR751) data are a part of 26 breast cell lines we analyzed.

2017-03-22 | PXD005390 | Pride

Desmocollin-1 is associated with pro-metastatic phenotype of luminal A breast cancer cells and is modulated by parthenolide

Project description:Desmocollin-1 is associated with pro-metastatic phenotype of luminal A breast cancer cells and is modulated by parthenolide

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The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was knocked down via siRNA in basal HCC1937 cell lines, in triplicate. Elf5 was induced in luminal T47D and MCF7 cell lines via a doxycycline inducible expression vector, in duplicate.

2012-12-27 | E-GEOD-30405 | biostudies-arrayexpress

Tumor Suppressor Role for the c-Myb Oncogene in Luminal Breast Cancer

Project description:The transcription factor c-Myb has been well characterized as an oncogene in several human tumor types, and its expression in the hematopoietic stem/progenitor cell population is essential for proper hematopoiesis. However, the role of c-Myb in mammopoeisis and breast tumorigenesis is poorly understood, despite its high expression in the majority of breast cancer cases (60-80%). We find that c-Myb high expression in human breast tumors correlates with the luminal/ER+ phenotype and a good prognosis. RNAi knock-down of endogenous c-Myb levels in the MCF7 luminal breast tumor cell line increases tumorigenesis both in vitro and in vivo, suggesting a tumor suppressor role in luminal breast cancer. We created a mammary-derived c-Myb expression signature and found it to be highly correlated with a published mature luminal mammary cell signature and least correlated with a mammary stem/progenitor lineage gene signature. These data describe, for the first time, a tumor suppressor role for the c-Myb proto-oncogene in breast cancer that has implications for understanding luminal tumorigenesis and for guiding treatment. refXsample

2010-10-15 | E-GEOD-21371 | biostudies-arrayexpress

Transcription factor activator protein 2C (TFAP2C) regulates luminal differentiation in mammary development and carcinogenesis

Project description:Molecular subtypes of breast cancer are characterized by patterns of gene expression, which can be used to predict response to therapy and overall clinical outcome. The luminal breast cancer subtypes are defined by the expression of ER-alpha (ERa) and a set of ERa-associated genes. The transcription factor activator protein 2C (TFAP2C, AP-2C, AP-2g) transcription factor plays a critical role in regulating cell growth and differentiation during ectodermal development and has been implicated in the regulation of ERa and other luminal-associated genes in breast cancer. While TFAP2C has been established as a prognostic factor in human breast cancer, the role of TFAP2C in development of the luminal epithelial cells in the normal mammary gland and in breast cancer have remained elusive. Herein, we demonstrate a critical role of TFAP2C in maintaining the luminal differentiation phenotype during normal mammary development and in luminal breast carcinoma cell lines. Total RNA from MCF7 cells with and without knockdown of TFAP2c. 3 biological replicates, with 2 technical replicates each, were performed for each sample type.

2014-02-01 | E-GEOD-44203 | biostudies-arrayexpress

Parthenolide-treated HeLa cells and purified tubulin

Project description:Purified human tubulin treated with parthenolide and HeLa cells treated in vivo with parthenolide

2021-01-22 | PXD020113 | Pride

Treatment of primary acute myelogenous leukemia (AML) specimens with parthenolide (PTL)

Project description:The effects of 7.5 micromolar parthenolide (PTL) were assessed on primary CD34+ acute myelogenous leukemia specimens obtained from 12 patients. Keywords: drug response, gene expression search agent

2008-02-27 | GSE7538 | GEO

Metabolomic Profiling Reveals Key Metabolic Alterations in MCF7 Tamoxifen-Resistant Cells Following EPAS1 Inhibition

Project description:<p>This study aims to investigate the metabolic alterations associated with acquired tamoxifen (TAM) resistance in luminal A breast cancer cells. Using untargeted LC-MS/MS metabolomics, we compared parental MCF7 and TAM-resistant MCF7/Tam1 cells to identify key metabolic pathways affected by EPAS1 (HIF-2α)-mediated hypoxia-driven reprogramming. The study further evaluates the impact of EPAS1 inhibition by PT2977 on the reversal of these metabolic changes and restoration of TAM sensitivity.</p>

2025-07-04 | MTBLS12677 | MetaboLights

Tumor Suppressor Role for the c-Myb Oncogene in Luminal Breast Cancer

Project description:BACKGROUND: The transcription factor c-Myb has been well characterized as an oncogene in several human tumor types, and its expression in the hematopoietic stem/progenitor cell population is essential for proper hematopoiesis. However, the role of c-Myb in mammopoeisis and breast tumorigenesis is poorly understood, despite its high expression in the majority of breast cancer cases (60-80%). METHODOLOGY/PRINCIPAL FINDINGS: We find that c-Myb high expression in human breast tumors correlates with the luminal/ER+ phenotype and a good prognosis. Stable RNAi knock-down of endogenous c-Myb in the MCF7 luminal breast tumor cell line increased tumorigenesis both in vitro and in vivo, suggesting a possible tumor suppressor role in luminal breast cancer. We created a mammary-derived c-Myb expression signature, comprised of both direct and indirect c-Myb target genes, and found it to be highly correlated with a published mature luminal mammary cell signature and least correlated with a mammary stem/progenitor lineage gene signature. CONCLUSIONS/SIGNIFICANCE: These data describe, for the first time, a possible tumor suppressor role for the c-Myb proto-oncogene in breast cancer that has implications for the understanding of luminal tumorigenesis and for guiding treatment.

2010-10-15 | GSE21371 | GEO

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