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KDM4 inhibition targets breast cancer stem cells [RNA-Seq]

ABSTRACT: We treated breast cancer stemm cells (BCSC) with a KDM4 inhibitor

ORGANISM(S): Homo sapiens

PROVIDER: GSE95293 | GEO | 2017/12/15

SECONDARY ACCESSION(S): PRJNA376575

REPOSITORIES: GEO

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KDM4 inhibition targets breast cancer stem cells [ChIP-Seq]

Project description:We treated breast cancer stemm cells (BCSC) with a KDM4 inhibitor or performed knockdown of KDM4A

2017-12-15 | GSE95190 | GEO

KDM4 inhibition targets breast cancer stem cells

Project description:Cancer progression is associated with alterations of epigenetic regulators such as histone-lysine demethylases 4 (KDM4)2-5. During breast cancer therapy, classical treatments fail to address resistant cancer stem cell populations6-10. Here, we identified a novel KDM4 inhibitor (KDM4(i)) with unique preclinical characteristics. KDM4(i) is a highly potent pan KDM4 inhibitor that specifically blocks the demethylase activity of KDM4A, B, C, and D but not that of the other members of the KDM family. We validated the KDM4(i) anti-tumoral properties under conditions recapitulating patient tumors. Therefore, we established a method to isolate and grow triple-negative breast cancer stem cells (BCSCs) from individual patient tumors after neoadjuvant chemotherapy. Limiting dilution orthotopic xenografts of these BCSCs faithfully regenerate original patient tumor histology and gene expression. KDM4(i) blocks proliferation, sphere formation and xenograft tumor growth of BCSCs. Importantly, KDM4(i) abrogates expression of EGFR, a driver of therapy-resistant triple-negative breast tumor cells11, via inhibition of the KDM4A demethylase activity. Taken together, we present a unique BCSC culture system as a basis for therapeutic compound identification and demonstrate that KDM4 inhibition is a new therapeutic strategy for the treatment of triple-negative breast cancer.

2018-04-10 | GSE95042 | GEO

KDM4 inhibition targets breast cancer stem cells

Project description:KDM4 inhibition targets breast cancer stem cells

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Understanding the impact of KDM4 inhibition on host cell processes

Project description:HepG2-NTCP cells were cultured in 1% oxygen or treated with a KDM4 inhibitor, QC6352, for 72 hours. RNA was extracted and the impact of treatment on the cellular transcriptome was investigated by RNA-sequencing.

2024-01-31 | GSE186279 | GEO

KDM4 inhibition targets breast cancer stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-12-15 | GSE95294 | GEO

Expression data from KDM4 inhibition

Project description:Expression data from KDM4 inhibition

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Expression data from tumor tissue-derived long-term-cultured breast cancer stem cells

Project description:Here we established two tumor tissue-derived long-term-cultured breast cancer stem cells (BCSC). RNA extraction and microarray analysis total RNA from BCSC treating with G1, G15, or control (Ctrl) for 48 hr were extracted using Trizol Reagent. Important significant differences of cDNA genes were identified. (The G1-treated group was designed as \\"12\\", the control group was \\"11\\" (raw data: 11 and 12; processed data: BCSC-G1). Similarly, the G15-treated study group was defined as \\"14\\", the control group was \\"13\\" (raw data: 13 and 14; processed data: BCSC-G15).

2017-09-04 | E-MTAB-5057 | biostudies-arrayexpress

Embryonic renal tumor cells sensitive to the small molecule inhibitor QC6352 display depletion of KDM4 levels and disruption of ribosome biogenesis-associated pathways

Project description:To investigate the effects of the KDM4 inhibitor QC6352 on embryonic renal tumor cells, we treated WiT49 anaplastic Wilms tumor cells and tumor-forming HEK293 human embryonic kidney cells with 25 nM QC6352 for 72 hours

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RNA-seq using RNA from KDM4 WT and Knockout haematopoietic stem cells

Project description:The KDM4/JMJD2 are H3K9- and H3K36- specific demethylases, which are considered promising therapeutic targets for the treatment of acute myeloid leukemia (AML) harboring MLL-translocations. Here, we investigate the long-term effects of depleting KDM4 activity on normal hematopoiesis to probe potential side effects of continuous inhibition of these enzymes. Utilizing conditional Kdm4a/Kdm4b/Kdm4c triple-knockout mice we show that KDM4 activity is required for hematopoietic stem cell (HSC) maintenance in vivo. The knockout of the KDM4 demethylases leads to accumulation of H3K9me3 on transcription start sites and the corresponding downregulation of expression of several genes in hematopoietic stem cells. We show that two of these genes, Taf1b and Nom1, are essential for the maintenance of hematopoietic cells. Taken together, our results show that the KDM4 demethylases are required for the expression of genes essential for the long-term maintenance of normal hematopoiesis.

2019-04-02 | GSE129137 | GEO

Paracrine Secretion of IL8 by Breast Cancer Stem Cells Promotes Therapeutic Resistance and Metastasis

Project description:Breast cancer stem cells (CSCs) play pivotal roles in cancer therapeutic failure and metastasis. However, it remains indeterminate how CSCs determine the progression of the bulk cancer cell population. Using a co-culture system in vitro and a co-implantation system in vivo, it is demonstrated herein that the breast cancer stem cell (BCSC) secretome rendered the bulk cancer cell population resistant to anti-estrogen and CDK4/6 inhibitor therapy; as well as increased the metastatic burden attributable to bulk cancer cells. Screening of BCSC secretome identified IL8 as a pivotal factor that potentiated ERα activity, endowed tamoxifen resistance and enhanced metastatic burden by regulation of bulk cancer cell behavior. Pharmacological inhibition of IL8 increased the efficacy of fulvestrant and/or palbociclib by reversing tamoxifen resistance and abrogated metastatic burden. Hence, this study has delineated the mechanism by which BCSCs determine the therapeutic response and metastatic of bulk cancer cells; and thereby suggests novel therapeutic strategies to ameliorate breast cancer outcomes.

2022-12-30 | GSE220295 | GEO

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