ArticleScientific reports2016
Thyrostimulin-TSHR signaling promotes the proliferation of NIH:OVCAR-3 ovarian cancer cells via trans-regulation of the EGFR pathway.
Article in Scientific reports, 2016. 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, 27 citations in OpenAlex.
- Extrathyroidal Expression of the Thyrotropin Receptor in Epithelial Cancer Cells.International journal of molecular sciences · 2026Article
- Resolved hyperthyroidism before IVF is not associated with improved cumulative live birth rates: a retrospective cohort study.Frontiers in endocrinology · 2026Article
- Molecular and Functional Insights into Thyrostimulin and Its Subunits-GPA2/GPB5.International journal of molecular sciences · 2025Review
- TSHR in thyroid cancer: bridging biological insights to targeted strategies.European thyroid journal · 2025Review
- Genome-Wide Detection for Runs of Homozygosity in Baoshan Pigs Using Whole Genome Resequencing.Genes · 2024Article
- A genomic region associated with iteroparous spawning phenology is linked with age-at-maturity in female steelhead trout.Evolutionary applications · 2024Article
- Opposing Effects of EGF Receptor Signaling on Proliferation and Differentiation Initiated by EGF or TSH/EGF Receptor Transactivation.Endocrinology · 2022Article
- The Mysterious Universe of the TSH Receptor.Frontiers in endocrinology · 2022Review
- Unconventional Actions of Glycoprotein Hormone Subunits: A Comprehensive Review.Frontiers in endocrinology · 2021Review
- Metabolic radiogenomics in lung cancer: associations between FDG PET image features and oncogenic signaling pathway alterations.Scientific reports · 2020Article
- The Molecular Function and Clinical Role of Thyroid Stimulating Hormone Receptor in Cancer Cells.Cells · 2020Review
- QuaDMutNetEx: a method for detecting cancer driver genes with low mutation frequency.BMC bioinformatics · 2020Article
- Expression Profiling, Downstream Signaling, and Inter-subunit Interactions of GPA2/GPB5 in the Adult MosquitoFrontiers in endocrinology · 2020Article
- Downregulation of lncRNA TUBA4B is Associated with Poor Prognosis for Epithelial Ovarian Cancer.Pathology oncology research : POR · 2018Article
- Cancer Stem Cells: Emergent Nature of Tumor Emergency.Frontiers in genetics · 2018Article
- Cytidine deaminase Apobec3a induction in fallopian epithelium after exposure to follicular fluid.Gynecologic oncology · 2017Article
- The Role of Endocrine G Protein-Coupled Receptors in Ovarian Cancer Progression.Frontiers in endocrinology · 2017Review
- Long noncoding RNA NBAT-1 suppresses tumorigenesis and predicts favorable prognosis in ovarian cancer.OncoTargets and therapy · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gonadotropin signaling plays an indispensable role in ovarian cancer progression. We previously have demonstrated that thyrostimulin and thyroid-stimulating hormone receptor (TSHR), the most ancient glycoprotein hormone and receptor pair that evolved much earlier than the gonadotropin systems, co-exist in the ovary. However, whether thyrostimulin-driven TSHR activation contributes to ovarian cancer progression in a similar way to gonadotropin receptors has never been explored. In this study, we first found that TSHR is expressed in both rat normal ovarian surface epithelium and human epithelial ovarian cancers (EOCs). Using human NIH:OVCAR-3 as a cell model, we demonstrated that thyrostimulin promotes EOC cell proliferation as strongly as gonadotropins. Thyrostimulin treatment not only activated adenylyl cyclase and the subsequent PKA, MEK-ERK1/2 and PI3K-AKT signal cascades, but also trans-activated EGFR signaling. Signaling dissection using diverse inhibitors indicated that EOC cell proliferation driven by thyrostimulin-TSHR signaling is PKA independent, but does require the involvement of the MEK-ERK and PI3K-AKT signal cascades, which are activated mainly via the trans-activation of EGFR. Thus, not only have we proved that this ancient glycoprotein hormone system is involved in NIH:OVCAR-3 cell proliferation for the first time, but also that it may possibly become a novel oncotarget when studying ovarian cancer.
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