ArticleMolecular cancer2010
Maximum growth and survival of estrogen receptor-alpha positive breast cancer cells requires the Sin3A transcriptional repressor.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Cross-ancestry GWAS meta-analysis identifies six breast cancer loci in African and European ancestry women.Nature communications · 2021Pooled it
- Switch-Independent 3A: An Epigenetic Regulator in Cancer with New Implications for Pulmonary Arterial Hypertension.Biomedicines · 2023Review
- Nuclear complement C3b promotes paclitaxel resistance by assembling the SIN3A/HDAC1/2 complex in non-small cell lung cancer.Cell death & disease · 2023Article
- Two assembly modes for SIN3 histone deacetylase complexes.Cell discovery · 2023Article
- Facts and prospects of peptide in targeted therapy and immune regulation against triple-negative breast cancer.Frontiers in immunology · 2023Review
- Suppression of SIN3A by miR-183 Promotes Breast Cancer Metastasis.Molecular cancer research : MCR · 2022Article
- Review
- Epigenetic readers and lung cancer: the rs2427964C>T variant of the bromodomain and extraterminal domain gene BRD3 is associated with poorer survival outcome in NSCLC.Molecular oncology · 2022Article
- Identification of Key Pathways and Genes in Obesity Using Bioinformatics Analysis and Molecular Docking Studies.Frontiers in endocrinology · 2021Article
- Repositioning of Antiparasitic Drugs for Tumor Treatment.Frontiers in oncology · 2021Review
- Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells.Oncotarget · 2017Article
- Sin3a regulates epithelial progenitor cell fate during lung development.Development (Cambridge, England) · 2017Article
- Sulforaphane-Induced Cell Cycle Arrest and Senescence are accompanied by DNA Hypomethylation and Changes in microRNA Profile in Breast Cancer Cells.Theranostics · 2017Article
- SIN3A and SIN3B differentially regulate breast cancer metastasis.Oncotarget · 2016Article
- Article
- Selective Inhibition of SIN3 Corepressor with Avermectins as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer.Molecular cancer therapeutics · 2015Article
- SIN3A, generally regarded as a transcriptional repressor, is required for induction of gene transcription by the aryl hydrocarbon receptor.The Journal of biological chemistry · 2014Article
- Alterations in the rat serum proteome induced by prepubertal exposure to bisphenol a and genistein.Journal of proteome research · 2014Article
- Sin3a acts through a multi-gene module to regulate invasion in Drosophila and human tumors.Oncogene · 2013Article
- Breast cancer proteome takes more than two to tango on TRAIL: beat them at their own game.The Journal of membrane biology · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSin3A is an evolutionarily conserved transcriptional repressor which regulates gene expression as part of the multi-protein Sin3 repressive complex. It functions as a scaffold upon which proteins with enzymatic activity dock, including chromatin modifying histone deacetylases. Although regulation of transcription by Sin3A has been studied in detail, little is understood about the function of Sin3A in cancer cells. We previously showed that Sin3A is expressed in breast cancer cells and is a repressor of estrogen receptor-alpha (ERα, ESR1) gene expression. Here, we expand our previous studies to elucidate the function of Sin3A in the control of gene expression and growth of breast cancer cells.
resultsAnalysis of gene expression following knockdown of Sin3A revealed changes in both basal and regulated gene transcription. Genes of known importance in breast cancer and estrogen signaling, including ERBB2, PGR, MYC, CLU, and NCOA2, were among those identified as Sin3A-responsive. The mechanism of Sin3A action varied among genes and was found to be mediated through both HDAC1/2 -dependent and -independent activities. Loss of Sin3A inhibited breast cancer cell growth by increasing apoptosis without affecting cell cycle progression. Analysis of both ERα-positive and ERα-negative cell lines revealed that the effects of Sin3A on growth were cell-type specific, as Sin3A expression promoted maximum growth of only the ERα-positive cells, and, notably, Sin3A protein itself was increased by estrogen. Further gene expression experiments revealed that Sin3A repressed expression of key apoptotic genes, including TRAIL, TRAILR1, CASP10, and APAF1, in ERα-positive, but not ERα-negative, cell lines, which could provide a mechanistic explanation for cell-type differences in growth.
conclusionsThis study identifies Sin3A as a regulator of gene expression, survival, and growth in ERα-positive breast cancer cells. Sin3A regulates the transcription of genes involved in breast cancer and apoptosis and acts through multiple mechanisms not limited to histone deacetylase function. These findings reveal previously undescribed functions of Sin3A in breast cancer and provide evidence for an important role of this transcriptional repressor in ERα-positive tumor cell growth.
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