KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA722302 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description: Not available
| S-EPMC8441056 | biostudies-literature
Project description:Epigenetics is critical for cell fate decision and contributes greatly to cancer initiation and development. However, the underlying mechanisms are still largely elusive, thus impeding the effective targeting of histone deacetylases (HDACs) for clinical cancer therapy. Here, We used RNA-seq to study potential targets of HDAC inhibitors for breast cancer therapy. And we performed RNA-seq assays in the MDA-MB-231 cell line treated separately with three HDAC inhibitors TSA, TDPA, FK228.
2021-09-22 | GSE172182 | GEO
Project description:As the most commonly diagnosed lung cancer, non–small cell lung carcinoma (NSCLC) is regulated by many long noncoding RNAs (lncRNAs). In the present study, we found that SH3PXD2A-AS1 expression in NSCLC tissues was upregulated compared with that in normal lung tissues in The Cancer Genome Atlas (TCGA) database by using the GEPIA website. K-M analysis was performed to explore the effects of this molecule on the survival rate in NSCLC. The results demonstrated that SH3PXD2A-AS1 expression was increased in human NSCLC, and high SH3PXD2A-AS1 expression was correlated with poor overall survival. SH3PXD2A-AS1 promotes lung cancer cell proliferation and accelerates cell cycle progression in vitro. Animal studies validated that knockdown of SH3PXD2A-AS1 inhibits NSCLC cell proliferation in vivo. Mechanically, SH3PXD2A-AS1 interacted with DHX9 to enhance FOXM1 expression, promote tumour cell proliferation and accelerate cell cycle progression. Altogether, SH3PXD2A-AS1 promoted NSCLC growth by interacting with DHX9 to enhance FOXM1 expression. SH3PXD2A-AS1 may serve as a promising predictive biomarker for the diagnosis and prognosis of patients with NSCLC.
2021-08-06 | GSE181195 | GEO
Project description:The rapid accumulation of self-renewed polarized microglia in the penumbra is the critical neuroinflammatory process after the onset of ischemic stroke, leading to secondary demyelination and neuronal loss. HDAC3 has been reported to regulate cell proliferation of tumour cells and modulate neuroinflammation. However, the mechanism by which HDAC3 regulates microgliosis and microglial polarization remains ambiguous. Herein, we demonstrated that microglia-specific ablation of HDAC3 (HDAC3-miKO) ameliorated poststroke long-term functional and histological outcomes. Starting with unbiased RNA seq of microglia, we identified mitosis as the most significant process reversed by loss of HDAC3. Notably, HDAC3-miKO specifically inhibited the proliferation of M1-like microglia but not M2-like microglia, resulting in microglial transition to an M1-like state. Moreover, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) revealed that HDAC3 deletion induced drastic closing of accessible regions enriched with motifs for PU.1. Taken together, we uncovered for the first time that HDAC3/PU.1-mediated differential proliferation-related reprogramming in different microglia populations drives poststroke inflammatory state transition of microglia and thereby contributes to the pathophysiology of ischemic stroke.
2024-03-13 | GSE220042 | GEO
Project description:The rapid accumulation of self-renewed polarized microglia in the penumbra is the critical neuroinflammatory process after the onset of ischemic stroke, leading to secondary demyelination and neuronal loss. HDAC3 has been reported to regulate cell proliferation of tumour cells and modulate neuroinflammation. However, the mechanism by which HDAC3 regulates microgliosis and microglial polarization remains ambiguous. Herein, we demonstrated that microglia-specific ablation of HDAC3 (HDAC3-miKO) ameliorated poststroke long-term functional and histological outcomes. Starting with unbiased RNA seq of microglia, we identified mitosis as the most significant process reversed by loss of HDAC3. Notably, HDAC3-miKO specifically inhibited the proliferation of M1-like microglia but not M2-like microglia, resulting in microglial transition to an M1-like state. Moreover, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) revealed that HDAC3 deletion induced drastic closing of accessible regions enriched with motifs for PU.1. Taken together, we uncovered for the first time that HDAC3/PU.1-mediated differential proliferation-related reprogramming in different microglia populations drives poststroke inflammatory state transition of microglia and thereby contributes to the pathophysiology of ischemic stroke.
2024-03-13 | GSE220041 | GEO
Project description:Long noncoding RNA SH3PXD2A-AS1 promotes NSCLC proliferation and accelerates cell cycle progression by interacting with DHX9
| PRJNA751041 | ENA
Project description:Cellular homeostasis is tightly linked to proliferation ensuring that only healthy cells divide. Homeostasis-sensing pathways including mTOR and integrated stress response (ISR) employ phosphorylation to regulate translation initiation and consequently cell cycle progression. Whether ubiquitin or ubiquitin-like molecules impact on translation and proliferation as part of existing or novel pathways is unknown. Here, we combine cell cycle screening, mass spectrometry and ribosome profiling to elucidate the molecular mechanism by which UFMylation, the modification of proteins with ubiquitin-fold modifier 1 molecules, controls translational homeostasis and cell cycle progression. Perturbation of UFMylation prevents eIF4F translation initiation complex assembly and recruitment of the ribosome. The ensuing global translational shutdown is sensed by cyclin D1 and halts the cell cycle independently of canonical ISR and mTOR signaling. Our findings establish UFMylation as a key regulator of translation that employs the principle of conserved cellular sensing mechanisms to couple translational homeostasis to cell cycle progression.
2022-03-23 | PXD015378 | Pride
Project description:The host cell cycle is a major target for manipulation by viral pathogens, which often replicate in certain cell cycle stages. The prevalent pathogen human cytomegalovirus (HCMV), for instance, only replicates during G1 and therefore employs diverse mechanisms for regulating cell cycle progression. Here, we demonstrate that the human enzyme sirtuin 2 (SIRT2) is required for HCMV-mediated cell cycle dysregulation. By combining virology assays with mass pectrometry-based proteome, acetylome, and interactome analyses, we have defined a pro-virus function for SIRT2 in regulating the G1 to S phase transition.
2023-10-13 | PXD041171 | Pride
Project description:Polymerase II pausing licenses cell-cycle progression
| PRJNA393887 | ENA
Project description:Chromatin modifiers play critical roles in epidermal development, but the functions of histone deacetylases in this context are poorly understood. We find that the Class I HDAC, HDAC3, is expressed broadly in embryonic epidermis, and is required for its orderly stepwise stratification. Stability of HDAC3 protein in vivo is reliant on NCoR and SMRT, which function redundantly in epidermal development. However, point mutations in the NCoR and SMRT Deacetylase Activating Domains, which are required for HDAC3’s enzymatic function, permit normal stratification, indicating that HDAC3’s roles in this context are independent of its histone deacetylase activity. HDAC3 functions both in conjunction with, and independent of, KLF4 to repress premature expression of different sets of terminal differentiation genes and suppresses expression of inflammatory cytokines through a RelA-dependent mechanism. These data identify HDAC3 as a hub coordinating multiple aspects of epidermal barrier acquisition. We used microarrays to determine transcriptional changes in Hdac3 deleted epidermis compared to control and Ncor1/Ncor2 deleted epidermis compared to control.
2020-08-23 | GSE137234 | GEO