ArticleMedicina (Kaunas, Lithuania)2019
Cell Cycle Arrest and Cytotoxic Effects of SAHA and RG7388 Mediated through p21
Article in Medicina (Kaunas, Lithuania), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Multimodal radiosensitization by hafnium oxide nanoparticles and HDAC inhibitors: mechanistic insights.Nanoscale advances · 2026Article
- CD24 and Mutant p53: Emerging Therapeutic Targets in Prostate Cancer Progression.Anti-cancer agents in medicinal chemistry · 2026Review
- MDM2 and DNMT1 inhibitors induce neuroblastoma cell death through p53-dependent and independent pathways.Epigenomics · 2025Article
- Regulation of PD-L1 Expression by SAHA-Mediated Histone Deacetylase Inhibition in Lung Cancer Cells.Cancers · 2025Article
- The effect of ubiquitination and deubiquitination to imatinib resistance in gastrointestinal stromal tumors.Frontiers in oncology · 2025Review
- Lactoferrin targeting INTL1 receptor inhibits hepatocellular carcinoma progression via apoptosis and cell cycle signaling pathways.Scientific reports · 2024Article
- MDM2: current research status and prospects of tumor treatment.Cancer cell international · 2024Review
- Emerging therapeutic strategies in cancer therapy by HDAC inhibition as the chemotherapeutic potent and epigenetic regulator.Medical oncology (Northwood, London, England) · 2024Review
- Article
- Rational design of synthetically tractable HDAC6/HSP90 dual inhibitors to destroy immune-suppressive tumor microenvironment.Journal of advanced research · 2023Article
- Gain of Function (GOF) Mutant p53 in Cancer-Current Therapeutic Approaches.International journal of molecular sciences · 2022Review
- Chidamide and venetoclax synergistically exert cytotoxicity on multiple myeloma by upregulating BIM expression.Clinical epigenetics · 2022Article
- SAHA induce hippo pathway in CCA cells without increasing cell proliferation.Molecular biology reports · 2022Article
- Transcription Factors as Novel Therapeutic Targets and Drivers of Prostate Cancer Progression.Frontiers in oncology · 2022Review
- Exploring novel capping framework: high substituent pyridine-hydroxamic acid derivatives as potential antiproliferative agents.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2021Article
- Article
- Vorinostat (SAHA) and Breast Cancer: An Overview.Cancers · 2021Review
- Effect of the HDAC Inhibitor on Histone Acetylation and Methyltransferases in A2780 Ovarian Cancer Cells.Medicina (Kaunas, Lithuania) · 2021Article
- Autophagy Inhibition Potentiates the Anticancer Effects of a Bendamustine Derivative NL-101 in Acute T Lymphocytic Leukemia.BioMed research international · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveAlterations in gene expressions are often due to epigenetic modifications that can have a significant influence on cancer development, growth, and progression. Lately, histone deacetylase inhibitors (HDACi) such as suberoylanilide hydroxamic acid (SAHA, or vorinostat, MK0683) have been emerging as a new class of drugs with promising therapeutic benefits in controlling cancer growth and metastasis. The small molecule RG7388 (idasanutlin, R05503781) is a newly developed inhibitor that is specific for an oncogene-derived protein called MDM2, which is also in clinical trials for the treatment of various types of cancers. These two drugs have shown the ability to induce p21 expression through distinct mechanisms in MCF-7 and LNCaP cells, which are reported to have wild-type TP53. Our understanding of the molecular mechanism whereby SAHA and RG7388 can induce cell cycle arrest and trigger cell death is still evolving. In this study, we performed experiments to measure the cell cycle arrest effects of SAHA and RG7388 using MCF-7 and LNCaP cells. MATERIALS AND
methodsThe cytotoxicity, cell cycle arrest, and apoptosis/necroptosis effects of the SAHA and RG7388 treatments were assessed using the Trypan Blue dye exclusion (TBDE) method, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, fluorescence assay with DEVD-amc substrate, and immunoblotting methods.
resultsThe RG7388 treatment was able to induce cell death by elevating p21
conclusionOur results from MCF-7 and LNCaP cells confirmed that SAHA and RG7388 treatments were able to induce cell death via a combination of cell cycle arrest and cytotoxic mechanisms. We speculate that our findings could lead to the development of newer treatments for breast and prostate cancers with drug combinations including HDACi.
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Registered trials
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