ArticleOncogene2009
PTEN deficiency accelerates tumour progression in a mouse model of thyroid cancer.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 93 citations in OpenAlex.
- P4HA2 promotes the progression of papillary thyroid cancer by enhancing degradation of IκBα to activate NF-κB signaling pathway.Cancer cell international · 2025Article
- NF-κB in Thyroid Cancer: An Update.International journal of molecular sciences · 2024Review
- Thyroid Hormone Receptors as Tumor Suppressors in Cancer.Endocrinology · 2024Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- E-cadherin on epithelial-mesenchymal transition in thyroid cancer.Cancer cell international · 2021Review
- Transcription Factor Profiling Identifies Spatially Heterogenous Mediators of Follicular Thyroid Cancer Invasion.Endocrine pathology · 2020Article
- Recommendations on Surveillance for Differentiated Thyroid Carcinoma in Children with PTEN Hamartoma Tumor Syndrome.European thyroid journal · 2020Review
- Review
- Steroid receptor coactivator-3 as a target for anaplastic thyroid cancer.Endocrine-related cancer · 2020Article
- Inflammation suppression prevents tumor cell proliferation in a mouse model of thyroid cancer.American journal of cancer research · 2020Article
- Triple-high expression of phosphatase and tensin homolog (PTEN), estrogen receptor (ER) and progesterone receptor (PR) may predict favorable prognosis for patients with Type I endometrial carcinoma.Journal of Cancer · 2020Article
- Multi-omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome.Cancers · 2019Review
- Coding Molecular Determinants of Thyroid Cancer Development and Progression.Endocrinology and metabolism clinics of North America · 2019Review
- Monocyte recruitment and activated inflammation are associated with thyroid carcinogenesis in a mouse model.American journal of cancer research · 2019Article
- Metformin and JQ1 synergistically inhibit obesity-activated thyroid cancer.Endocrine-related cancer · 2018Article
- MicroRNA-146b promotes PI3K/AKT pathway hyperactivation and thyroid cancer progression by targeting PTEN.Oncogene · 2018Article
- Mechanisms Linking Obesity and Thyroid Cancer Development and Progression in Mouse Models.Hormones & cancer · 2018Review
- The Role of the Transcription Factor Nuclear Factor-kappa B in Thyroid Autoimmunity and Cancer.Frontiers in endocrinology · 2018Review
- Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor β.Molecular carcinogenesis · 2017Article
- Inhibition of STAT3 signaling blocks obesity-induced mammary hyperplasia in a mouse model.American journal of cancer research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Inactivation and silencing of PTEN have been observed in multiple cancers, including follicular thyroid carcinoma. PTEN (phosphatase and tensin homologue deleted from chromosome 10) functions as a tumour suppressor by opposing the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling pathway. Despite correlative data, how deregulated PTEN signalling leads to thyroid carcinogenesis is not known. Mice harbouring a dominant-negative mutant thyroid hormone receptor beta (TRbeta(PV/PV) mice) spontaneously develop follicular thyroid carcinoma and distant metastases similar to human cancer. To elucidate the role of PTEN in thyroid carcinogenesis, we generated TRbeta(PV/PV) mice haploinsufficient for Pten (TRbeta(PV/PV)Pten(+/-) mouse). PTEN deficiency accelerated the progression of thyroid tumour and increased the occurrence of metastasis spread to the lung in TRbeta(PV/PV)Pten(+/-) mice, thereby significantly reducing their survival as compared with TRbeta(PV/PV)Pten(+/+) mice. AKT activation was further increased by two-fold in TRbeta(PV/PV)Pten(+/-) mice thyroids, leading to increased activity of the downstream mammalian target of rapamycin (mTOR)-p70S6K signalling and decreased activity of the forkhead family member FOXO3a. Consistently, cyclin D1 expression was increased. Apoptosis was decreased as indicated by increased expression of nuclear factor-kappaB (NF-kappaB) and decreased caspase-3 activity in the thyroids of TRbeta(PV/PV)Pten(+/-) mice. Our results indicate that PTEN deficiency resulted in increased cell proliferation and survival in the thyroids of TRbeta(PV/PV)Pten(+/-) mice. Altogether, our study provides direct evidence to indicate that in vivo, PTEN is a critical regulator in the follicular thyroid cancer progression and invasiveness.
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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.