ArticleCarcinogenesis2013
Crosstalk between lysine-specific demethylase 1 (LSD1) and histone deacetylases mediates antineoplastic efficacy of HDAC inhibitors in human breast cancer cells.
Article in Carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 112 citations in OpenAlex.
- Inhibition of histone demethylase LSD1 suppresses CD47 expression and enhances efficacy of CD47 blockade in breast cancer.Journal for immunotherapy of cancer · 2026Article
- Corin: a dual inhibitor for KDM1A/HDAC1, suppresses hepatocellular carcinoma by triggering cuproptosis.Clinical and experimental medicine · 2025Article
- Mechanistic insights into novel cyano-pyrimidine pendant chalcone derivatives as LSD1 inhibitors by docking, ADMET, MM/GBSA, and molecular dynamics simulation.Biochemistry and biophysics reports · 2025Article
- Lysine specific demethylase 1 conditional myeloid cell knockout mice have decreased osteoclast differentiation due to increased IFN-JBMR plus · 2025Article
- Syntheses of LSD1/HDAC Inhibitors with Demonstrated Efficacy against Colorectal Cancer:Journal of medicinal chemistry · 2024Article
- Restoration of TFPI2 by LSD1 inhibition suppresses tumor progression and potentiates antitumor immunity in breast cancer.Cancer letters · 2024Article
- The emerging roles of histone demethylases in cancers.Cancer metastasis reviews · 2024Review
- Apigenin and its combination with Vorinostat induces apoptotic-mediated cell death in TNBC by modulating the epigenetic and apoptotic regulators and related miRNAs.Scientific reports · 2024Article
- Article
- Interaction between host cell proteins and open reading frames of porcine circovirus type 2.Journal of animal science and technology · 2023Review
- Targeting the LSD1/KDM1 Family of Lysine Demethylases in Cancer and Other Human Diseases.Advances in experimental medicine and biology · 2023Review
- Novel dual LSD1/HDAC6 inhibitor for the treatment of cancer.PloS one · 2023Article
- Pharmacological Inhibition of Lysine-Specific Demethylase 1A Reduces Atherosclerotic Lesion Formation in Apolipoprotein E-Deficient Mice by a Mechanism Involving Decreased Oxidative Stress and Inflammation; Potential Implications in Human Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- Cancer-Cell-Selective Targeting by Arylcyclopropylamine-Vorinostat Conjugates.ACS medicinal chemistry letters · 2022Article
- Targeting Histone Epigenetic Modifications and DNA Damage Responses in Synthetic Lethality Strategies in Cancer?Cancers · 2022Article
- Article
- A state-of-the-art review on LSD1 and its inhibitors in breast cancer: Molecular mechanisms and therapeutic significance.Frontiers in pharmacology · 2022Review
- Reactive Oxygen Species-Mediated Mitochondrial Dysfunction Triggers Sodium Valproate-Induced Cytotoxicity in Human Colorectal Adenocarcinoma Cells.Journal of gastrointestinal cancer · 2021Article
- Arborinine, a potential LSD1 inhibitor, inhibits epithelial-mesenchymal transition of SGC-7901 cells and adriamycin-resistant gastric cancer SGC-7901/ADR cells.Investigational new drugs · 2021Article
- Analysis framework and experimental design for evaluating synergy-driving gene expression.Nature protocols · 2021Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Our previous studies demonstrated that lysine-specific demethylase 1 (LSD1) and histone deacetylases (HDACs) closely interact in controlling growth of breast cancer cells. However, the underlying mechanisms are largely unknown. In this study, we showed that knockdown of LSD1 expression (LSD1-KD) by RNAi decreased mRNA levels of HDAC isozymes in triple-negative breast cancer (TNBC) cells. Small interfering RNA (siRNA)-mediated depletion of HDAC5 expression induced the most significant accumulation of H3K4me2, a specific substrate of LSD1. Combined treatment with LSD1 inhibitor, pargyline, and HDAC inhibitor, SAHA (Vorinostat), led to superior growth inhibition and apoptotic death in TNBC cells, but exhibited additive or antagonistic effect on growth inhibition in non-TNBC counterparts or non-tumorigenic breast cells. Additionally, LSD1-KD enhanced SAHA-induced reexpression of a subset of aberrantly silenced genes, such as NR4A1, PCDH1, RGS16, BIK, and E-cadherin whose reexpression may be tumor suppressive. Genome-wide microarray study in MDA-MB-231 cells identified a group of tumor suppressor genes whose expression was induced by SAHA and significantly enhanced by LSD1-KD. We also showed that concurrent depletion of RGS16 by siRNA reduced overall cytotoxicity of SAHA and blocked the reexpression of E-cadherin, CDKN1C and ING1 in LSD1-deficient MDA-MB-231 cells. Furthermore, cotreatment with RGS16 siRNA reversed the downregulation of nuclear factor-kappaB expression induced by combined inhibition of LSD1 and HDACs, suggesting a crucial role of RGS16 in controlling key pathways of cell death in response to combination therapy. Taken together, these results provide novel mechanistic insight into the breast cancer subtype-dependent role of LSD1 in mediating HDAC activity and therapeutic efficacy of HDAC inhibitor.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.