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Transcription profiling of human chondrosarcoma cells resistant to ET-743 and PM00104

ABSTRACT: ET-743 (trabectedin, YondelisÂ®) and PM00104 (ZalypsisÂ®) are marine derived compounds that have antitumor activity. ET-743 and PM00104 exposure over sustained periods of treatment will result in the development of drug resistance, but the mechanisms which lead to resistance are not yet understood. Human chondrosarcoma cell lines resistant to ET-743 (CS-1/ER) or PM00104 (CS-1/PR) were established in this study. The CS-1/ER and CS-1/PR exhibited cross resistance to cisplatin and methotrexate but not to doxorubicin. Human Affymetrix Gene Chip arrays were used to examine relative gene expression in these cell lines. Experiment Overall Design: Three samples CS-1/ER, CS-1/PR and CS-1 were compared.

ORGANISM(S): Homo sapiens

SUBMITTER: Zhenfeng Duan

PROVIDER: E-GEOD-16748 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from human chondrosarcoma cells resistance to ET-743 and PM00104

Project description:ET-743 (trabectedin, Yondelis®) and PM00104 (Zalypsis®) are marine derived compounds that have antitumor activity. ET-743 and PM00104 exposure over sustained periods of treatment will result in the development of drug resistance, but the mechanisms which lead to resistance are not yet understood. Human chondrosarcoma cell lines resistant to ET-743 (CS-1/ER) or PM00104 (CS-1/PR) were established in this study. The CS-1/ER and CS-1/PR exhibited cross resistance to cisplatin and methotrexate but not to doxorubicin. Human Affymetrix Gene Chip arrays were used to examine relative gene expression in these cell lines.

2009-06-24 | GSE16748 | GEO

Gene and microRNA modulation upon ET-743 treatment in a human intrahepatic cholangiocarcinoma paired patient derived xenograft and cell line [gene expression]

Project description:Transcriptional profiling and microRNA profiling of paired PDX and derived cell line MT-CHC01 upon ET-743 treatement Intrahepatic cholangiocarcinoma (ICC) is an aggressive and lethal malignancy with limited therapeutic options. ET-743 has a high antitumor activity in preclinical models of biliary tract carcinoma (BTC), being a promising alternative treatment. Here, we studied the effect of ET-743 at transcriptomic level on an ICC patient derived xenograft (PDX) and on the derived cell line, MT-CHC01. Further, putative targets of ET-743 were explored in the in vitro model. In vitro, ET-743 inhibited genes involved in protein modification, neurogenesis, migration, and motility; it induced the expression of genes involved in keratinization, tissues development, and apoptotic processes. In the PDX model, ET-743 affected ECM-receptor interaction, focal adhesion, complement and coagulation cascades, Hedgehog, MAPK, EGFR signaling via PIP3 pathway, and apoptosis. In MT-CHC01, 24 microRNAs were deregulated upon drug treatment. Only 5 microRNAs were perturbed by ET-743 in PDX; 2 up and 3 down-regulated. Among down- regulated genes, we selected SYK and LGALS1; their silencing caused a significantly reduction of migration, but did not affect proliferation in MT-CHC01 and WITT cells. In conclusion, we described that ET-743 affected genes and microRNAs involved in tumor progression and metastatic processes, reflecting data previously obtained at macroscopically level; in particular, we identified SYK and LGALS1 as new putative targets of ET-743.

2017-06-10 | GSE84918 | GEO

Gene and microRNA modulation upon ET-743 treatment in a human intrahepatic cholangiocarcinoma paired patient derived xenograft and cell line [miRNA expression]

2017-06-10 | GSE84938 | GEO

Transcriptional profiling of patient-derived xenograft models of myxoid liposarcoma either responsive or resistant to trabectedin treatment.

Project description:Transcriptional profiling of patient-derived xenograft models of myxoid liposarcoma with either FUS-CHOP type I, named as ML017, or FUS-CHOP type III, named as ML006. Both ML017 and ML006 are responsive to trabectedin treatment, while model ML017/ET has aquired resistance to the drug. Samples are either under untreated conditions, or treated either with trabectedin or pioglitazone or both.

2020-01-10 | E-MTAB-8632 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data from human chondrosarcoma cells resistance to ET-743 and PM00104

| PRJNA117449 | ENA

Gene expression profiling of dendritic cells in different physiological stages under Cordyceps sinensis treatment

Project description:Cordyceps sinensis (CS) has been commonly used as a herbal medicine as well as a health supplement in China for over two thousand years. Although previous studies demonstrated that CS has benefit in immunoregulation and anti-inflammation, the precise mechanism by which CS affects immunomodulation is still unclear. In this study, we adopted duplicate sets of loop-design microarray experiments to examine two different batches of CS and analyzed the effects of CS on dendritic cells (DCs) in different physiology stages, naïve stage and inflammatory stage. We used duplicate sets of loop-design microarray in this study. Each loop experiment consisted of 4 RNA samples, including untreated samples, CS 1μg/ml, LPS 1μg/ml, and LPS 1μg/ml+ CS 1μg/ml.

2011-09-08 | E-GEOD-24191 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [ChIP-seq]

Project description:Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations. Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers.

2016-06-01 | GSE80367 | GEO

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [cell models RNA-seq]

2016-06-01 | GSE80366 | GEO

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [tumor samples RNA-seq]

2016-06-01 | GSE80365 | GEO

SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner

Project description:Luminal breast cancers express estrogen (ER) and progesterone (PR) receptors, and respond to endocrine therapies. However, some ER+PR+ tumors display intrinsic or acquired resistance, possibly related to PR. Two PR isoforms, PR-A and PR-B, regulate distinct gene subsets that may differentially influence tumor fate. A high PR-A:PR-B ratio is associated with poor prognosis and tamoxifen resistance. We speculate that excessive PR-A marks tumors that will relapse early. Here we address mechanisms by which PR-A regulate transcription, focusing on SUMOylation. We use receptor mutants and synthetic promoter/reporters to show that SUMOylation deficiency or the deSUMOylase SENP1 enhance transcription by PR-A, independent of the receptors’ dimerization interface or DNA binding domain. De-SUMOylation exposes the agonist properties of the antiprogestin RU486. Thus, on synthetic promoters, SUMOylation functions as an independent brake on transcription by PR-A. What about PR-A SUMOylation of endogenous human breast cancer genes? To study these, we used gene expression profiling. Surprisingly, PR-A SUMOylation influences progestin target genes differentially, with some upregulated, others downregulated, and others unaffected. Hormone-independent gene regulation is also PR-A SUMOylation dependent. Several SUMOylated genes were analyzed in clinical breast cancer database. In sum, we show that SUMOylation does not simply repress PR-A. Rather, it regulates PR-A activity in a target selective manner including genes associated with poor prognosis, shortened survival, and metastasis.

2018-02-02 | GSE108607 | GEO

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