Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Heparins treated human breast cancer MCF-7 cell

ABSTRACT: To inquire the a possible mechanism for heparin treatment improved cancer survival, three type of heparins: one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane were used to treat cell for 24 hours. Total RNA was used for cDNA Microarray assay. Untreated cells were used as controls. Cell were treated by three type of heparins one standard heparin (unfractionated heparin (UFH), and two of low molecular weight heparin (LMWH) Fragmin and Clexane (40 IU/ml for each) were used to treat cell for 24 hours. Triplicate samples were prepared.

ORGANISM(S): Homo sapiens

SUBMITTER: Yunliang Chen Chen

PROVIDER: E-GEOD-26537 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Radiation and chemotherapy represent standard-of-care cancer treatments, however most treated patients eventually experience tumor recurrence, treatment failure and metastatic dissemination with fatal consequences. To elucidate molecular mechanisms of resistance to radio- and chemo-therapy, we exposed human cancer cell lines (HeLa, MCF-7, and DU145) to clinically relevant doses of 5-azacytidine or ionizing radiation and compared the transcript profiles of all surviving cell subpopulations including non-adherent fraction. Stress-mobilized non-adherent cell fractions differed from other survivors in deregulation of hundreds of genes including those involved in interferon response. Exposure of cancer cells to interferon-gamma but not interferon-beta resulted in development of a heterogeneous non-adherent fraction comprising, besides apoptotic/necrotic cells, also live cells featuring active Notch signaling and expressing stem cell markers. Interferon-gamma-mediated loss of adhesion and anoikis-resistance required active Erk pathway interlinked with interferon signaling by IRF1, as chemical inhibition of MEK or siRNA-mediated knockdown of Erk1/2 and IRF1 prevented mobilization of the surviving non-adherent population. Noteworthy, among the top scoring genes upregulated in surviving non-adherent tumor cells induced by 5-azacytidine or irradiation was a skin-specific protein suprabasin (SBSN), a recently identified oncoprotein. SBSN expression required the activity of the MEK/Erk pathway, and siRNA-mediated knockdown of SBSN resulted in suppression of the non-adherent fraction in irradiated, interferon-gamma- and 5-azacytidine-treated cells, respectively. Consistently, ectopic expression of SBSN isoforms enhanced the non-adherent phenotype, suggesting functional participation of SBSN in genotoxic stress-induced phenotypic plasticity and stress resistance. The stress-induced expression of skin protein(s) in a subset of cancer cells indicates partial induction of a keratinocyte-like expression program. Overall, we propose that IFN and Erk signaling drive the heterogeneous response of cancer cells to genotoxic therapies and expression of keratinocyte-specific genes as key players in mobilization and survival of cancer stem-like cells, with implications for cancer evolution and therapy resistance.

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Heparins treated human breast cancer MCF-7 cell

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