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Unknown,Transcriptomics,Genomics,Proteomics

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Isolation of subtype-specific N-Ras responsive genes in basal-like breast cancer cells

ABSTRACT: To identify the the N-Ras-controlled genes in basal-like cells, we used shRNA to repress N-RAS in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells. We seek the genes regulated only in basal-like, but not in claudin-low cells, to isolate the genes controlled by N-Ras in a breast cancer subtype-specific fashion. We also overexpressed oncogenic form N-Ras(G12D) in these cells in order to compare the genes regulated by wild-type and oncogenic N-Ras. The shRNA silencing and overexpression were conducted by lentiviral infection in the cells, with non-silencing shRNA-infected cells as the controls. The infected cells were then selected in antibiotics for about 5 days before total RNAs were harvested for microarray analysis. N-Ras was silenced by shRNA or oncogenic N-Ras (G12D) was overexpressed in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Eric Chang

PROVIDER: E-GEOD-61768 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Isolation of subtype-specific N-Ras responsive genes in basal-like breast cancer cells

Project description:To identify the the N-Ras-controlled genes in basal-like cells, we used shRNA to repress N-RAS in basal-like SUM102PT, SUM149PT and claudin-low SUM159PT cells. We seek the genes regulated only in basal-like, but not in claudin-low cells, to isolate the genes controlled by N-Ras in a breast cancer subtype-specific fashion. We also overexpressed oncogenic form N-Ras(G12D) in these cells in order to compare the genes regulated by wild-type and oncogenic N-Ras. The shRNA silencing and overexpression were conducted by lentiviral infection in the cells, with non-silencing shRNA-infected cells as the controls. The infected cells were then selected in antibiotics for about 5 days before total RNAs were harvested for microarray analysis.

2015-06-06 | GSE61768 | GEO

Characterization of Cell Lines Derived from Breast Cancers and Normal Mammary Tissues for the Study of the Intrinsic Molecular Subtypes

Project description:Five molecular subtypes (Luminal A/B, HER2-enriched, Basal-like, and Claudin-low) with clinical implications have been identified. In this report, we evaluated molecular and phenotypic relationships of a large in vitro panel of human breast cancer cell lines (BCCLs), human mammary fibroblasts (HMFs) and human mammary epithelial cells (HMECs) with (1) breast tumors, (2) normal breast cell-enriched subpopulations and (3) human embryonic stem cells (hESCs) and bone marrow-derived mesenchymal stem cells (hMSC). First, by integrating genomic data of 337 breast samples with 93 cell lines we were able to identify all the intrinsic tumor subtypes in vitro, except for the Luminal A. Secondly, we observed that cell lines recapitulate the differentiation hierarchy observed in the mammary gland, with Claudin-low BCCLs and HMFs cells showing a stromal phenotype, HMECs showing a mammary stem cell/bipotent progenitor phenotype, Basal-like cells showing a luminal progenitor phenotype, and Luminal B cells showing a luminal phenotype. Thirdly, we identified Basal-like and highly migratory Claudin-low subpopulations of cells within a subset of triple-negative BCCLs (SUM149PT, HCC1143 and HCC38). Interestingly, both subpopulations within SUM149PT where found to have Tumor Initiating Cell (TIC) features, but the Basal-like subpopulation grew faster than the Claudin-low subpopulation. Finally, Claudin-low BCCLs were found to resemble the phenotype of hMSCs, whereas hESCs cells were found to have an epithelial phenotype without basal and luminal differentiation. The results presented here should help improve our understanding of the cell line model system through the appropriate pairing of cell lines with relevant in vivo tumor and normal cell counterparts. reference x sample

2013-10-29 | E-GEOD-50470 | biostudies-arrayexpress

Gene expression profile at single cell level of SUM149PT, SUM185PE, SUM229PE, SUM159PT and SUM1315MO2 cell lines

Project description:SUM149PT, SUM185PE, SUM229PE, SUM159PT and SUM1315MO2 are triple negative breast cancer cell lines. They were sequenced to test the contrastive learning-based algorithm we developed to predict Afatinib sensitivity in TNBC.

2024-03-25 | GSE228275 | GEO

Characterization of Cell Lines Derived from Breast Cancers and Normal Mammary Tissues for the Study of the Intrinsic Molecular Subtypes

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N-Linked Glycoprotein Profiles of Human Breast Basal 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 nine basal malignant breast cells (HCC1143, HCC1395, HCC1937, HCC1954, HCC38, HCC70, MDAMB468, SUM149PT and SUM229PE) data are a part of 26 breast cell lines we analyzed.

2017-03-27 | PXD005295 | Pride

EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [human]

Project description:The newly identified claudin-low subtype of cancer is believed to represent the most primitive breast malignancies, having arisen from transformation of an early epithelial precursor with inherent stemness properties and metaplastic features. Challenging this hypothesis, we show both in vitro and in vivo that transcription factors inducing epithelial-mesenchymal transition can drive the development of claudin-low tumors from differentiated mammary epithelial cells, by playing a dual role in cell transformation and dedifferentiation. Human mammary epithelial cells (HMEC) were sequentially immortalized by hTert (HMEC-hTert), transduced with Twist1 or Zeb2 or Zeb1 and then with H-RasG12V. The gene expression profiles of the resulting HMEC-hTert-Twist1+Ras, HMEC-hTert-Zeb1+Ras and HMEC-hTert-Zeb2+Ras cell lines were defined. HMEC-hTert-Twist1+Ras and HMEC-hTert-Zeb2+Ras cell lines were additionally cultured in presence of TGFM-CM-^C? and their gene expression profiles were determined. The parental HMEC-hTert, the luminal MCF7 and the basal B MDMB157cell lines were used as controls.

2012-07-23 | E-GEOD-32727 | biostudies-arrayexpress

Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT

Project description:Transcriptional profiling of mouse lung tumors comparing Dnmt3a KO/K-ras G12D mutant with Dnmt3a WT/K-ras G12D mutant. The goal is to search for the difference of mRNA abundance between Dnmt3a KO and WT tumors. Two-condition experiment, KO vs. WT tissure. Biological replicates: 12.

2011-10-25 | E-GEOD-32415 | biostudies-arrayexpress

Highly metastatic claudin-low mammary cancers can originate from luminal epithelial cells

Project description:Claudin-low breast cancer represents an aggressive molecular subtype that is comprised of mostly triple-negative mammary tumor cells that possess stem cell-like and mesenchymal features. Little is known about the cellular origin and oncogenic drivers that promote claudin-low breast cancer. In this study, we show that persistent oncogenic RAS signaling causes highly metastatic triple-negative mammary tumors in mice. More importantly, the activation of endogenous mutant KRAS and expression of exogenous KRAS specifically in luminal epithelial cells in a continuous and differentiation stage-independent manner induces preneoplastic lesions that evolve into basal-like and claudin-low mammary cancers. Further investigations demonstrate that the continuous signaling of oncogenic RAS as well as regulators of EMT play a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.

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Mouse lung tumor tissue: Dnmt3a KO vs. Dnmt3a WT

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Targeted mass spectrometry analyses of somatic mutations in colorectal cancer specimens using differential ion mobility

Project description:Identification of K-Ras and B-Raf mutations in colorectal cancer (CRC) is essential to predict patients' response to anti-EGFR therapy and formulate appropriate therapeutic strategies to improve prognosis and survival. Here, we combined parallel reaction monitoring (PRM) with high-field asymmetric waveform ion mobility (FAIMS) to enhance mass spectrometry sensitivity and improve the identification of low-abundance K-Ras and B-Raf mutations in biological samples without immunoaffinity enrichment. In targeted LC-MS/MS analyses, FAIMS reduced the occurrence of interfering ions and enhanced precursor ion purity, resulting in a three-fold improvement in the detection limit for K-Ras and B-Raf mutated peptides. In addition, ion mobility separation of isomeric peptides using FAIMS facilitated the unambiguous identification of K-Ras G12D and G13D peptides. The application of targeted LC-MS/MS analyses using FAIMS is demonstrated for the detection and quantitation of B-Raf V600E, K-Ras G12D, G13D, and G12V in CRC cell lines and primary specimens.

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