ArticleBMC cancer2021
NR1D1 suppressed the growth of ovarian cancer by abrogating the JAK/STAT3 signaling pathway.
Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- The circadian architecture of tumor immunity: mechanistic insights and treatment strategies.Biomarker research · 2026Review
- REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Circadian clock and cancer.Military Medical Research · 2026Review
- NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.Mediators of inflammation · 2026Article
- Functional role of circadian clock system in steroidogenesis and cell death pathways during corpus luteum regression in cattle.Cell and tissue research · 2025Article
- Discovery of Natural Compound α-Hederin via Large-Scale Screening as a Targeted JAK/STAT3 Inhibitor for Ovarian Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Circadian patterns of growth factor receptor-dependent signaling and implications for carcinogenesis.Cell communication and signaling : CCS · 2024Review
- Low expression of NR1D1 and NR2E3 is associated with advanced features of retinoblastoma.International ophthalmology · 2024Article
- Review
- Nuclear receptors in ovarian cancer: changing paradigms in cancer therapeutics.Frontiers in oncology · 2024Review
- NR1D1 Stimulates Antitumor Immune Responses in Breast Cancer by Activating cGAS-STING Signaling.Cancer research · 2023Article
- NR1D1 deficiency in the tumor microenvironment promotes lung tumor development by activating the NLRP3 inflammasome.Cell death discovery · 2023Article
- Expression and Localization of Fas-Associated Factor 1 in Testicular Tissues of Different Ages and Ovaries at Different Reproductive Cycle Phases ofAnimals : an open access journal from MDPI · 2023Article
- E2F3 accelerates the stemness of colon cancer cells by activating the STAT3 pathway.Frontiers in oncology · 2023Article
- MYCL promotes the progression of triple‑negative breast cancer by activating the JAK/STAT3 pathway.Oncology reports · 2022Article
- A novel tumor mutational burden-based risk model predicts prognosis and correlates with immune infiltration in ovarian cancer.Frontiers in immunology · 2022Article
- Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNuclear receptor subfamily 1 group D member 1 (NR1D1), a nuclear receptor associated with a variety of physiological processes, has a low level in ovarian cancer tissues compared with adjacent normal tissues. However, its role in ovarian cancer remains unclear.
methodsThe level of NR1D1 in ovarian cancer cells was determined by quantitative real-time PCR. Its role in ovarian cancer was explored through gain-of-function and lose-of-function. Cell growth was evaluated by CCK8 assay, immunofluorescence and flow cytometry. Western blot was conducted to assess the activation of JAK/STAT3 signaling pathway. A xenograft model of ovarian cancer was established to explore the role of NR1D1 in vivo.
resultsUp-regulation of NR1D1 repressed the ovarian cancer cell proliferation and induced cell cycle arrest and apoptosis, while silencing NR1D1 promoted their proliferation and G1/S transition. In addition, the JAK/STAT3 signaling pathway, an intracellular signal transduction closely associated with cancer progression, was inhibited by NR1D1. Consistently, xenografts with NR1D1 over-expression grew more slowly in vivo than the controls. Furthermore, NR1D1 up-regulated the expression of suppressor of cytokine signaling 3 (SOCS3), an inhibitor of the JAK/STAT3 signaling pathway. Whereas, SOCS3 silencing abolished the function of NR1D1 over-expression on ovarian cancer growth and JAK/STAT3 signaling pathway.
conclusionsNR1D1 up-regulated the expression of SOCS3, resulting in suppression of the JAK/STAT3 signaling pathway, thus retarding the growth of ovarian cancer cells. This study highlights a profound role of NR1D1 in the treatment of ovarian cancer.
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