ArticleOncogene2004
P21(WAF1/CIP1) is dispensable for G1 arrest, but indispensable for apoptosis induced by sodium butyrate in MCF-7 breast cancer cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 97 citations in OpenAlex.
- Stabilization of cyclin D3 protein by CDKN1A (p21Cell communication and signaling : CCS · 2026Article
- Targeting microbiome-driven epigenetic modifications: a new frontier in breast cancer treatment.Clinical epigenetics · 2026Review
- Insights into the gut microbiome-metabolite dynamics in breast cancer.Gut microbes reports · 2025Review
- Exploring the impact of breast cancer on colonization resistance of mouse microbiota using network node manipulation.Heliyon · 2024Article
- Mechanistic Insights into the Anti-Proliferative Action of Gut Microbial Metabolites against Breast Adenocarcinoma Cells.International journal of molecular sciences · 2023Article
- Gut Metabolites and Breast Cancer: The Continuum of Dysbiosis, Breast Cancer Risk, and Potential Breast Cancer Therapy.International journal of molecular sciences · 2022Review
- Potential of histone deacetylase inhibitors in the control and regulation of prostate, breast and ovarian cancer.Frontiers in chemistry · 2022Review
- Short-Chain Fatty Acid Butyrate Induces Cilia Formation and Potentiates the Effects of HDAC6 Inhibitors in Cholangiocarcinoma Cells.Frontiers in cell and developmental biology · 2021Article
- Review
- Histone Deacetylases and Histone Deacetylase Inhibitors: Molecular Mechanisms of Action in Various Cancers.Advanced biomedical research · 2019Review
- Effect of sodium butyrate on cell proliferation and cell cycle in porcine intestinal epithelial (IPEC-J2) cells.In vitro cellular & developmental biology. Animal · 2017Article
- Epigenetics in Intestinal Epithelial Cell Renewal.Journal of cellular physiology · 2016Review
- The histone deacetylase inhibitor trichostatin a decreases lymphangiogenesis by inducing apoptosis and cell cycle arrest via p21-dependent pathways.BMC cancer · 2016Article
- Histone deacetylase inhibition impairs normal intestinal cell proliferation and promotes specific gene expression.Journal of cellular biochemistry · 2015Article
- Transcriptional repression of histone deacetylase 3 by the histone demethylase KDM2A is coupled to tumorigenicity of lung cancer cells.The Journal of biological chemistry · 2014Article
- Recruitment of trimeric proliferating cell nuclear antigen by G1-phase cyclin-dependent kinases following DNA damage with platinum-based antitumour agents.British journal of cancer · 2013Article
- Human rpL3 induces G₁/S arrest or apoptosis by modulating p21 (waf1/cip1) levels in a p53-independent manner.Cell cycle (Georgetown, Tex.) · 2013Article
- Lycorine induces cell-cycle arrest in the G0/G1 phase in K562 cells via HDAC inhibition.Cancer cell international · 2012Article
- Efficacy of the dietary histone deacetylase inhibitor butyrate alone or in combination with vitamin A against proliferation of MCF-7 human breast cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012Article
- Plant HDAC inhibitor chrysin arrest cell growth and induce p21WAF1 by altering chromatin of STAT response element in A375 cells.BMC cancer · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium butyrate (NaB) has been proposed as a potential anticancer agent. However, its mechanism of action is not totally elucidated. Here, we showed that NaB-induced cell cycle arrest and apoptosis were associated with an increase of P21(waf1/cip1) in MCF-7 breast cancer cells. This increase was more important in the nuclei, as revealed by immunofluorescence analysis. Transient transfections of MCF-7 cells with p21 deficient for interaction with CDK, but not with p21 deficient for interaction with PCNA (p21PCNA-), abrogated NaB-induced cell cycle arrest. This indicated that cell cycle blockage involved the interaction of P21(waf1/cip1) with CDK. However, P21(waf1/cip1) was dispensable, since p21 antisense did not modify cell cycle arrest. On the other hand, NaB-induced apoptosis was abolished by p21 antisense or p21PCNA-. In addition, NaB decreased PCNA levels, but increased the association of PCNA with P21(waf1/cip1). These results suggested that NaB-induced apoptosis required P21(waf1/cip1) and its interaction with PCNA.
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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.