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Gene expression profiling of human neuroblastoma cell line BE(2)-C with inducible KDM4C expression

ABSTRACT: The microarray gene expression profiling reveals that the histone H3 demethylase KDM4C transcriptionally activates the serine-glycine pathway, stress responses and genes in control of cell-cycle progression. Affymetrix microarray assays were performed according to the manufacturer's directions on total RNA isolated from three independent samples of BE(2)-C_tetoff_KDM4C cells cultured in the presence or absence of doxycycline for 6 days.

ORGANISM(S): Homo sapiens

SUBMITTER: Justin Choi

PROVIDER: E-GEOD-65966 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiling of BIX01294-treated human neuroblastoma cell line BE(2)-C

Project description:Increased activation of the serine-glycine biosynthetic pathway is an integral part of cancer metabolism that drives macromolecule synthesis needed for cell proliferation. Whether this pathway is under epigenetic control is unknown. Here we show that the histone H3 lysine 9 (H3K9) methyltransferase G9A is required for maintaining the pathway enzyme genes in an active state marked by H3K9 monomethylation and for the transcriptional activation of this pathway in response to serine deprivation. G9A inactivation depletes serine and its downstream metabolites, triggering cell death with autophagy in cancer cell lines of different tissue origins. Higher G9A expression, which is observed in various cancers and is associated with greater mortality in cancer patients, increases serine production and enhances the proliferation and tumorigenicity of cancer cells. These findings identify a G9A-dependent epigenetic program in the control of cancer metabolism, providing a rationale for G9A inhibition as a therapeutic strategy for cancer. Affymetrix microarray assays were performed according to the manufacturer's directions on total RNA isolated from three independent samples of BE(2)-C cells treated either with 0.05% DMSO or with 5 M-BM-5M BIX01294 (B9311, Sigma-Aldrich) for 24 hours.

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Gene expression profiling of human neuroblastoma cell line BE(2)-C with inducible KDM4C expression

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KDM4C epigenetically regulates and forms a feed-forward loop with ALDH1A3 to maintain gastric cancer stemness

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Expression data of KDM4C knockout by CRISPR in Prostate cancer cell line C4-2B

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The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (ChIP-seq ESCs)

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Gene expresion changes following knockdown of KDM4C in primary fibroblasts

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USP9X-mediated KDM4C deubiquitination promotes lung cancer radioresistance by epigenetically inducing TGFβ2 transcription

Project description:Radioresistance is regarded as the main barrier to effective radiotherapy in lung cancer. However, the underlying mechanisms of radioresistance remain elusive. Here, we show that lysine-specific demethylase 4C (KDM4C) is overexpressed and correlated with poor prognosis in lung cancer patients. We provide evidence that genetical or pharmacological inhibition of KDM4C impairs tumorigenesis and radioresistance in lung cancer in vitro and in vivo. Moreover, we uncover that KDM4C upregulates TGFβ2 expression by directly reducing H3K9me3 level at the TGFβ2 promoter and then activates TGF-β/Smad/ATM signaling to confer radioresistance in lung cancer. Using tandem affinity purification technology, we further identify deubiquitinase USP9X as a critical binding partner which deubiquitinates and stabilizes KDM4C. More importantly, depletion of USP9X impairs TGF-β/Smad signaling and radioresistance by destabilizing KDM4C in lung cancer cells. Thus, our findings demonstrate that USP9X-mediated KDM4C deubiquitination activates TGF-β/Smad signaling to promote radioresistance, suggesting that targeting KDM4C may be a promising radiosensitization strategy in the treatment of lung cancer.

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