ArticleCancer communications (London, England)2021
KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression.
Article in Cancer communications (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Construction and Multi-dimensional Validation of a Lactylation-Related Signature for Glioblastoma Multiforme Prognostic and Therapeutic Purposes.Molecular biotechnology · 2026Article
- Dual epigenetic and nuclear export inhibition by chidamide and selinexor in high grade B-cell lymphomas via survivin and PI3K/AKT inhibition.Clinical epigenetics · 2026Article
- A pan-cancer analysis of the oncogenic role of KDELR2 in human cancers.Discover oncology · 2025Article
- Chidamide and anlotinib synergistically inhibit high grade B-cell lymphomas via PI3K/AKT signaling pathway.Scientific reports · 2025Article
- Signalling pathways and cellular functions of KDEL receptors: implications in cancer biology.Cellular and molecular life sciences : CMLS · 2025Review
- Construction and validation of acetylation-related gene signatures for immune landscape analysis and prognostication risk prediction in luminal breast cancer.Cancer cell international · 2025Article
- Large-scale bulk and single-cell RNA sequencing combined with machine learning reveals glioblastoma-associated neutrophil heterogeneity and establishes a VEGFABiology direct · 2025Article
- Review
- KDELR3 overexpression as a novel prognostic and diagnostic biomarker in glioma: comprehensive bioinformatic analysis insights.Scientific reports · 2024Article
- Multimodal single cell-resolved spatial proteomics reveal pancreatic tumor heterogeneity.Nature communications · 2024Article
- Exploring the potential biological significance of KDELR family genes in lung adenocarcinoma.Scientific reports · 2024Article
- HDAC inhibitors target IRS4 to enhance anti‑AR therapy in AR‑positive triple‑negative breast cancer.International journal of oncology · 2024Article
- A pancancer analysis of histone deacetylase 3 in human tumors.Translational cancer research · 2024Article
- A new perspective on macrophage-targeted drug research: the potential ofFrontiers in immunology · 2024Article
- LowTranslational cancer research · 2023Article
- Identification of co-expressed gene networks promoting CD8BMC ophthalmology · 2023Article
- Genetic Variants Associated with Longitudinal Cognitive Performance in Older Breast Cancer Patients and Controls.Cancers · 2023Article
- HDAC3 Inhibition Promotes Antitumor Immunity by Enhancing CXCL10-Mediated Chemotaxis and Recruiting of Immune Cells.Cancer immunology research · 2023Article
- The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases.Cell death discovery · 2023Review
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Authors and funding
15 authors.
Funding
Abstract
backgroundHistone deacetylases (HDACs) engage in the regulation of various cellular processes by controlling global gene expression. The dysregulation of HDACs leads to carcinogenesis, making HDACs ideal targets for cancer therapy. However, the use of HDAC inhibitors (HDACi) as single agents has been shown to have limited success in treating solid tumors in clinical studies. This study aimed to identify a novel downstream effector of HDACs to provide a potential target for combination therapy.
methodsTranscriptome sequencing and bioinformatics analysis were performed to screen for genes responsive to HDACi in breast cancer cells. The effects of HDACi on cell viability were detected using the MTT assay. The mRNA and protein levels of genes were determined by quantitative reverse transcription-PCR (qRT-PCR) and Western blotting. Cell cycle distribution and apoptosis were analyzed by flow cytometry. The binding of CREB1 (cAMP-response element binding protein 1) to the promoter of the KDELR (The KDEL (Lys-Asp-Glu-Leu) receptor) gene was validated by the ChIP (chromatin immunoprecipitation assay). The association between KDELR2 and protein of centriole 5 (POC5) was detected by immunoprecipitation. A breast cancer-bearing mouse model was employed to analyze the effect of the HDAC3-KDELR2 axis on tumor growth.
resultsKDELR2 was identified as a novel target of HDAC3, and its aberrant expression indicated the poor prognosis of breast cancer patients. We found a strong correlation between the protein expression patterns of HADC3 and KDELR2 in tumor tissues from breast cancer patients. The results of the ChIP assay and qRT-PCR analysis validated that HDAC3 transactivated KDELR2 via CREB1. The HDAC3-KDELR2 axis accelerated the cell cycle progression of cancer cells by protecting the centrosomal protein POC5 from proteasomal degradation. Moreover, the HDAC3-KDELR2 axis promoted breast cancer cell proliferation and tumorigenesis in vitro and in vivo.
conclusionOur results uncovered a previously unappreciated function of KDELR2 in tumorigenesis, linking a critical Golgi-the endoplasmic reticulum traffic transport protein to HDAC-controlled cell cycle progression on the path of cancer development and thus revealing a potential therapeutical target for breast cancer.
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