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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Effect of lestaurtinib on KM-H2 HRS cell line

ABSTRACT: Effect of the tyrosine kinase inhibitor (TKI) lestaurtinib on Hodgkin and Reed/Sternberg (HRS) cell line KM-H2 compared to the solvent treated control.

ORGANISM(S): Homo sapiens

SUBMITTER: Meike Holz

PROVIDER: E-MEXP-3565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Induction of endoplasmic reticulum stress by sorafenib and activation of NF-κB by lestaurtinib as a novel resistance mechanism in Hodgkin lymphoma cell lines.

Holz Meike Stefanie MS Janning Angela A Renné Christoph C Gattenlöhner Stefan S Spieker Tilmann T Bräuninger Andreas A

Molecular cancer therapeutics 20121213 2

Hodgkin-Reed/Sternberg (HRS) cells of classical Hodgkin lymphoma show aberrant expression and activation of several receptor tyrosine kinases (RTK) in the majority of cases. Therefore, we tested whether tyrosine kinase inhibitors (TKI) already in clinical use or late stages of clinical trials have antiproliferative effects on HRS cell lines and evaluated the targets, affected signaling pathways, and mechanisms of cell death and resistance. Sorafenib and lestaurtinib had antiproliferative effects ...[more]

PMID: 23243060

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Expression changes induced by PTPN1 knockdown in KM-H2 cells

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2014-01-17 | E-GEOD-54157 | biostudies-arrayexpress

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Gene expression profiling of cell lines derived from classical Hodgkin lymphoma

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. To determine differentially expressed genes between Hodgkin Reed Sternberg cells and their presumed cell of origin we investigated the expression profiles of 5 commonly used Hodgkin lymphoma cell lines as compared to reactive germinal centers.

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Project description:FOXO1 is highly expressed in normal B cells and in most types of non-Hodgkinl lymphoma. In Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma(cHL) expression of FOXO1 is low or absent. We overexpressed constitutively active mutant of FOXO1 fused in frame with estrogen receptor ligand-binding domain (FOXO1(3A)ER), which can be activated by 4-Hydroxytamoxifen (4-OHT), in cHL cell lines KM-H2 and L428. Activation of the FOXO1 with 4-OHT resulted in inhibition of proliferation and apoptosis. Using gene-expression array we found that FOXO1 activates transcription of known and potential tumor suppressor genes: CDKN1B, PMAIP1, BCL2L11, TNFSF10, FBXO32, CBLB). Of note, FOXO1 repressed transcription of several cytokines and cytokine receptors, which are known tobe involved in pathogenesis of cHL (e.g. CCL5, CXCR5, TNFRSF8). Taken togather our data indicate important role of FOXO1 repression in pathogenesis of cHL. KM-H2 and L428 cells expressing constitutively active mutant of human FOXO1 fused in frame with estrogen receptor ligand-binding domain were incubated with 200 ÂµM 4-OHT or vehicle (ethanol). After 24 h, total RNA was isolated with RNeasy mini kit (QIAGEN). Microarray analyses were performed using 200 ng of total RNA as starting material and 5.5 Âµg ssDNA per hybridization (GeneChip Fluidics Station 450; Affymetrix, Santa Clara, CA). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (http://www.affymetrix.com). Labeled ssDNA was hybridized to Human Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix, Santa Clara, CA). The chips were scanned with a Affymetrix GeneChip Scanner 3000 and subsequent images analyzed using AffymetrixÂ® Expression Console Software (Affymetrix). Probe level data were obtained using the robust multichip average (RMA) normalization algorithm.

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