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A novel histone deacetylases inhibitor exerts promising anti-breast cancer activity via triggering AIFM1-dependent programmed necrosis

ABSTRACT: A novel histone deacetylases inhibitor exerts promising anti-breast cancer activity via triggering AIFM1-dependent programmed necrosis

PROVIDER: PRJNA838191 | ENA |

REPOSITORIES: ENA

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A novel histone deacetylases inhibitor exerts promising anti-breast cancer activity via triggering AIFM1-dependent programmed necrosis

Project description:Breast cancer is one of the most lethal cancers in women, and its resistance to chemotherapy remains a challenging problem. Histone deacetylases inhibitors (HDACIs) are a promising therapeutic tool for breast cancer. Here, we screened a library of synthetic small molecules and identified a novel HDACi, YF349, which possessed promising anti-breast cancer ability both in vitro and in vivo. Molecular and biochemical studies demonstrated that YF349 significantly increased the mRNA level of apoptosis-inducing factor (AIFM1) by blocking the binding of HDAC1 to the AIFM1 promoter. Further study revealed that YF349 significantly induced nuclear translocation of AIFM1 and promoted the formation of the AIF-CypA-gH2Ax complex in the nuclei, finally inducing AIF-mediated necrosis. Our finding suggests that AIFM1 can be explored as a molecular target in breast cancer and that targeting the HDAC1-AIFM1-CypA-gH2Ax signaling axis by YF349 may be a promising therapeutic strategy for breast cancer. We identified a novel compound for breast cancer therapy

2022-11-16 | GSE203025 | GEO

A novel histone deacetylase inhibitor exerts promising anti-breast cancer activity via triggering AIFM1-dependent programmed necrosis.

Project description: Not available

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Dosage dependent tumor suppression by histone deacetylases 1/2

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Function of histone deacetylases on fission yeast heterochromatin assembly

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Cold priming and triggering of Arabidopsis accessions

Project description:Cold priming and triggering of Arabidopsis accessions

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Cold priming and triggering of Arabidopsis accessions

Project description:Plants from temperate regions can be primed by exposure to low, non-freezing temperatures resulting in improved freezing tolerance. Whereas the molecular and metabolic basis of cold priming has been investigated in detail, hardly anything is known about memory of a previous cold event under warm conditions and a following low temperature triggering event. We show that three days of cold priming at 4°C, a seven-day lag phase at 20°C and a triggering treatment of 4°C improved the freezing tolerance of Arabidopsis Col-0 and other accessions compared to plants that were not primed before. Transcripts, metabolites and lipids as possible molecular determinants of this increase in freezing tolerance were investigated in Arabidopsis accessions Col-0 and N14 after priming, memory phase and triggering by Illumina-based RNA-Seq, GC-MS metabolite profiling and UPLC FT-MS-based lipidomics. Comparing primed and triggered with only triggered samples 93 and 128 unique differentially expressed genes could be identified in Col-0 and N14, together with three and six significantly changed lipids and one metabolite in N14. Possible functions of these candidates will be discussed. This work identified for the first time molecular and metabolic changes accompanying cold stress memory and triggering by a second cold stress.

2019-01-31 | GSE112225 | GEO

Class I histone deacetylases HDAC1, 2 and 3 are histone decrotonylases

Project description:We characterize histone crotonylation in intestinal epithelium-derived cells through Mass spectrometry, ChIp-Seq and RNA-Seq approaches and show that this modification is removed by class I histone deacetylases, HDAC1, 2 and 3.

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Regulation of Tumor Progression by Programmed Necrosis.

Project description:Rapidly growing malignant tumors frequently encounter hypoxia and nutrient (e.g., glucose) deprivation, which occurs because of insufficient blood supply. This results in necrotic cell death in the core region of solid tumors. Necrotic cells release their cellular cytoplasmic contents into the extracellular space, such as high mobility group box 1 (HMGB1), which is a nonhistone nuclear protein, but acts as a proinflammatory and tumor-promoting cytokine when released by necrotic cells. These released molecules recruit immune and inflammatory cells, which exert tumor-promoting activity by inducing angiogenesis, proliferation, and invasion. Development of a necrotic core in cancer patients is also associated with poor prognosis. Conventionally, necrosis has been thought of as an unregulated process, unlike programmed cell death processes like apoptosis and autophagy. Recently, necrosis has been recognized as a programmed cell death, encompassing processes such as oncosis, necroptosis, and others. Metabolic stress-induced necrosis and its regulatory mechanisms have been poorly investigated until recently. Snail and Dlx-2, EMT-inducing transcription factors, are responsible for metabolic stress-induced necrosis in tumors. Snail and Dlx-2 contribute to tumor progression by promoting necrosis and inducing EMT and oncogenic metabolism. Oncogenic metabolism has been shown to play a role(s) in initiating necrosis. Here, we discuss the molecular mechanisms underlying metabolic stress-induced programmed necrosis that promote tumor progression and aggressiveness.

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