ArticleOncogene2011
Akt1 deficiency delays tumor progression, vascular invasion, and distant metastasis in a murine model of thyroid cancer.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- In silico discovery of natural and synthetic inhibitors targeting AKT1 in prostate cancer.Molecular diversity · 2026Article
- Investigating the potential anti-cancer mechanism for thyroid cancer: Role of Herba Epimedii via network pharmacology approach.Journal, genetic engineering & biotechnology · 2025Article
- Pathogenesis of cancers derived from thyroid follicular cells.Nature reviews. Cancer · 2023Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- Novel Inhibitor-Based Therapies for Thyroid Cancer-An Update.International journal of molecular sciences · 2021Review
- Targeting Akt in cancer for precision therapy.Journal of hematology & oncology · 2021Review
- Transcriptome analysis discloses dysregulated genes in normal appearing tumor-adjacent thyroid tissues from patients with papillary thyroid carcinoma.Scientific reports · 2021Article
- AGTR1 Inhibits the Progression of Lung Adenocarcinoma.Cancer management and research · 2021Article
- Akt isoform-specific effects on thyroid cancer development and progression in a murine thyroid cancer model.Scientific reports · 2020Article
- The unconventional role of Akt1 in the advanced cancers and in diabetes-promoted carcinogenesis.Pharmacological research · 2019Review
- Akt1 inhibition promotes breast cancer metastasis through EGFR-mediated β-catenin nuclear accumulation.Cell communication and signaling : CCS · 2018Article
- mTOR Pathway in Papillary Thyroid Carcinoma: Different Contributions of mTORC1 and mTORC2 Complexes for Tumor Behavior andInternational journal of molecular sciences · 2018Article
- Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia.Molecular and cellular endocrinology · 2018Article
- Article
- RCAN1-4 is a thyroid cancer growth and metastasis suppressor.JCI insight · 2017Article
- Coupling of LETM1 up-regulation with oxidative phosphorylation and platelet-derived growth factor receptor signaling via YAP1 transactivation.Oncotarget · 2016Article
- Mouse models of thyroid cancer: A 2015 update.Molecular and cellular endocrinology · 2016Review
- Inhibition of breast cancer invasion by TIS21/BTG2/Pc3-Akt1-Sp1-Nox4 pathway targeting actin nucleators, mDia genes.Oncogene · 2016Article
- Review
- Follicular thyroid cancers demonstrate dual activation of PKA and mTOR as modeled by thyroid-specific deletion of Prkar1a and Pten in mice.The Journal of clinical endocrinology and metabolism · 2014Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Akt activation is common in progressive thyroid cancer. In breast cancer, Akt1 induces primary cancer growth, but is reported to inhibit metastasis in vivo in several model systems. In contrast, clinical and in vitro studies suggest a metastasis-promoting role for Akt1 in thyroid cancer. The goal of this study was to determine the functional role of Akt1 in thyroid cancer growth and metastatic progression in vivo using thyroid hormone receptor (TR) β(PV/PV) knock-in (PV) mice, which develop metastatic thyroid cancer. We crossed Akt1(-/-) and PV mice and compared tumor development, local progression, metastasis and histology in TRβ(PV/PV)/Akt1(+/+) (PVPV-Akt1WT) and TRβ(PV/PV)/Akt1(-/-) (PVPV-Akt1KO) mice. Mice were killed at 3, 6, 9, 12 and 15 months; necropsy was performed and serum thyroid stimulating hormone (TSH) was measured. Thyroid hyperplasia occurred in both groups beginning at 3 months; the thyroid size was greater in the PVPV-Akt1WT mice (P<0.001). In comparison with PVPV-Akt1WT mice, thyroid cancer development was delayed in the PVPV-Akt1KO mice (P=0.003) and the degree of tumor invasiveness was reduced. The PVPV-Akt1WT mice displayed pulmonary metastases at 12 and 15 months of age, by contrast PVPV-Akt1KO mice did not develop distant metastases at 15 months of age. Despite continued expression of Akt2 or Akt3, pAkt levels were decreased and there was evidence of reduced Akt effect on p27 in the PVPV-Akt1KO thyroids. TSH levels were similarly elevated in PV mice regardless of Akt1 expression. In conclusion, thyroid cancer development and progression in TR β(PV/PV) mice are Akt1-dependent, consistent with a tumor progression-promoting role in this murine thyroid cancer model.
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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.