ArticleCancer research2023
ESRRB Inhibits the TGFβ Signaling Pathway to Drive Cell Proliferation in Cervical Cancer.
Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury.Journal of advanced research · 2026Article
- Emerging landscape of oncogenic signaling pathways in cervical cancer.Discover oncology · 2026Review
- Tumor cell cycle regulation: integrated perspective of stage characteristics, regulatory networks, and signaling pathway intervention strategies.Molecular biomedicine · 2026Review
- Calcium and Cadmium Activate ESRRB to Mediate Cell Stemness and Pluripotency.International journal of molecular sciences · 2025Article
- A preserved TGFβ cytostatic response through DLD-mediated metabolic modulation undermines anti-TGFβ therapy in gastric cancer.Nature communications · 2025Article
- Granulocyte colony-stimulating factor induced T-cell hyporesponsiveness via modulation of CD177Clinical and translational medicine · 2025Article
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Human Papillomavirus and Other Relevant Issues in Cervical Cancer Pathogenesis.International journal of molecular sciences · 2025Review
- CDKN1A as a potential target for Eltrombopag treatment in ITP and its regulation of the communication between macrophages and transitional B cells in ITP.Annals of hematology · 2025Article
- Expression and prognostic value of estrogen-related receptor β alternative splicing isoforms in esophageal squamous cell carcinoma.European journal of medical research · 2025Article
- Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.Journal of hematology & oncology · 2025Review
- Chorionic trophoblast cells demonstrate functionally different phenotypes from placental trophoblasts†.Biology of reproduction · 2025Article
- ZEB2 upregulation modulates the polarization of TAMs toward the immunosuppressive state in EGFR-TKI-resistant NSCLC.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- The Role of the Vaginal Microbiome in Immune Modulation in Cervical Cancer: Composition, Molecular Mechanisms, and Therapeutic Potential.Clinical Medicine Insights. Oncology · 2025Review
- Targeting cancer stem cells by TPA leads to inhibition of refractory sarcoma and extended overall survival.Molecular therapy. Oncology · 2024Article
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- Functional pathogenicity of ESRRB variant of uncertain significance contributes to hearing loss (DFNB35).Scientific reports · 2024Article
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Dual disease co-expression analysis reveals potential roles of estrogen-related genes in postmenopausal osteoporosis and Parkinson's disease.Frontiers in genetics · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen-related receptor β (ESRRB) is a member of the orphan nuclear receptor family and mediates stem cell self-renewal and early embryonic development. Previous studies have also reported that ESRRB plays a role in the development and progression of breast cancer and prostate cancer. In this study, we observed that ESRRB was highly expressed in cervical cancer and was associated with disease progression. Knocking out ESRRB using CRISPR/Cas9 gene editing in cervical cancer cells induced cell-cycle arrest at the transition from the G0-G1 phase to the S phase, resulting in inhibition of cell proliferation in vitro and reduced tumor growth in vivo. Conversely, ectopic expression of ESRRB significantly promoted the proliferation of cervical cancer cells. ESRRB activated transcription of SMAD7, a TGFβ pathway inhibitor, which blocked phosphorylation and nuclear translocation of SMAD2/3 to the nucleus, thereby downregulating CDKN1A and upregulating CCNA2 and MYC. In turn, MYC transactivated ESRRB and upregulated SMAD7, thus forming a positive feedback loop with ESRRB. Together, these findings identify the tumor-promoting function of ESRRB in cervical cancer and reveal a mechanism by which ESRRB stimulates cell proliferation to promote cancer progression. SIGNIFICANCE: The ESRRB/SMAD7/MYC-positive feedback loop inhibits TGFβ signaling to activate cell-cycle progression and promote proliferation in cervical cancer, thereby driving tumor growth.
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Registered trials
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.