ArticleCell death & disease2018
Checkpoint suppressor 1 suppresses transcriptional activity of ERα and breast cancer cell proliferation via deacetylase SIRT1.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Survival and Clinicopathological Significance of SIRT1 Expression in Cancers: A Meta-Analysis.Frontiers in endocrinology · 2019Pooled it
- The clinical and prognostic significance of FOXN3 downregulation in acute myeloid leukaemia.International journal of laboratory hematology · 2020Trial
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- The exosomal miRNA/FOXN3 axis empowers fibroblasts with tumor-promoting functions via enhanced migration and altered secretome.Journal of nanobiotechnology · 2026Article
- The role of the SIRT1/FOXO1 axis in regulating autophagy and inflammation in endometriosis.Journal of translational medicine · 2026Article
- All the Way: A Decade of SIRT1 in Breast Cancer.Biomedicines · 2026Review
- Emerging Targeted and Multimodal Therapeutic Strategies in Breast Cancer: A Comprehensive Review.Breast cancer (Dove Medical Press) · 2026Review
- Review
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
- Hypoxia-triggered ERRα acetylation enhanced its oncogenic role and promoted progression of renal cell carcinoma by coordinating autophagosome-lysosome fusion.Cell death & disease · 2025Article
- USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- FOXN3 inhibits the progression of ovarian cancer through negatively regulating the expression of RPS15A.Human cell · 2023Article
- Acetylation of Checkpoint suppressor 1 enhances its stability and promotes the progression of triple-negative breast cancer.Cell death discovery · 2022Article
- FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma.Aging · 2021Article
- Trending topics of SIRT1 in tumorigenicity.Biochimica et biophysica acta. General subjects · 2021Review
- SIRT1 and gynecological malignancies (Review).Oncology reports · 2021Review
- Acetylation of ELF5 suppresses breast cancer progression by promoting its degradation and targeting CCND1.NPJ precision oncology · 2021Article
- SRC Promotes Tamoxifen Resistance in Breast Cancer via Up-Regulating SIRT1.OncoTargets and therapy · 2020Article
- Breaking down the Contradictory Roles of Histone Deacetylase SIRT1 in Human Breast Cancer.Cancers · 2018Review
- SIRT1 and Estrogen Signaling Cooperation for Breast Cancer Onset and Progression.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is a highly heterogeneous carcinoma in women worldwide, but the underlying mechanisms that account for breast cancer initiation and development have not been fully established. Mounting evidence indicates that Checkpoint suppressor 1 (CHES1) is tightly associated with tumorigenesis and prognosis in many types of cancer. However, the definitive function of CHES1 in breast cancer remains to be explored. Here we showed that CHES1 had a physical interaction with estrogen receptor-α (ERα) and repressed the transactivation of ERα in breast cancer cells. Mechanistically, the interaction between CHES1 and ERα enhanced the recruitment of nicotinamide adenine dinucleotide (NAD+) deacetylase Sirtuin 1 (SIRT1), and it further induced SIRT1-mediated ERα deacetylation and repression on the promoter-binding enrichment of ERα. In addition, we also found that the expression of CHES1 was repressed by estrogen-ERα signaling and the expression level of CHES1 was significantly downregulated in ERα-positive breast cancer. The detailed mechanism was that ERα may directly bind to CHES1 potential promoter via recognizing the conserved estrogen response element (ERE) motif in response to estrogen stimulation. Functionally, CHES1 inhibited ERα-mediated proliferation and tumorigenesis of breast cancer cells in vivo and in vitro. Totally, these results identified a negative cross-regulatory loop between ERα and CHES1 that was required for growth of breast cancer cells, it might uncover novel insight into molecular mechanism of CHES1 involved in breast cancer and provide new avenues for molecular-targeted therapy in hormone-regulated breast cancer.
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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.