ArticleCancer research2016
Aberrant Activation of Notch Signaling Inhibits PROX1 Activity to Enhance the Malignant Behavior of Thyroid Cancer Cells.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 40 citations in OpenAlex.
- The roles of both the endogenous synthesis and exogenous uptake of fatty acids in thyroid cancer cell proliferation.European journal of medical research · 2025Article
- PROX1 Expression in Resected Non-Small Cell Lung Cancer: Immunohistochemical Profile and Clinicopathological Correlates.Medical sciences (Basel, Switzerland) · 2025Article
- Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Characteristics and advances in signaling pathways, cellular communication, cell junctions, and oxidative stress in lymphedema.Frontiers in cell and developmental biology · 2025Review
- Immune response and mesenchymal transition of papillary thyroid carcinoma reflected in ultrasonography features assessed by radiologists and deep learning.Journal of advanced research · 2024Article
- The Role of Lipid Metabolism Disorders in the Development of Thyroid Cancer.International journal of molecular sciences · 2024Review
- The role of MAPK, notch and Wnt signaling pathways in papillary thyroid cancer: Evidence from a systematic review and meta-analyzing microarray datasets employing bioinformatics knowledge and literature.Biochemistry and biophysics reports · 2024Article
- Prox1 Suppresses the Proliferation of Breast Cancer Cells via Direct Inhibition of c-Myc Gene Expression.Cells · 2023Article
- lncRNA EGFEM1P promotes thyroid cancer progression by acting as an miR-369-3p sponge and upregulating TCF4.Oncology letters · 2022Article
- The Role of PROX1 in Neoplasia: A Key Player Often Overlooked.Diagnostics (Basel, Switzerland) · 2022Review
- SLC8A1 antisense RNA 1 suppresses papillary thyroid cancer malignant progression via the FUS RNA binding protein (FUS)/NUMB like endocytic adaptor protein (Numbl) axis.Bioengineered · 2022Article
- Abnormal activation of notch 1 signaling causes apoptosis resistance in cervical cancer.International journal of clinical and experimental pathology · 2022Article
- Cell and Molecular Biology of Thyroid Disorders 2.0.International journal of molecular sciences · 2021Article
- Notch Signaling in Thyroid Cancer.Advances in experimental medicine and biology · 2021Review
- The Role of LINC00284 in the Development of Thyroid CancerFrontiers in oncology · 2021Article
- YAP and TAZ maintain PROX1 expression in the developing lymphatic and lymphovenous valves in response to VEGF-C signaling.Development (Cambridge, England) · 2020Article
- Identification of key genes of papillary thyroid carcinoma by integrated bioinformatics analysis.Bioscience reports · 2020Article
- The Lymphatic Cell Environment Promotes Kaposi Sarcoma Development by Prox1-Enhanced Productive Lytic Replication of Kaposi Sarcoma Herpes Virus.Cancer research · 2020Article
- The Impact of Transcription Factor Prospero Homeobox 1 on the Regulation of Thyroid Cancer Malignancy.International journal of molecular sciences · 2020Review
- miR-934 as a Prognostic Marker Facilitates Cell Proliferation and Migration of Pancreatic Tumor by Targeting PROX1.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
31 authors at 6 institutions in 3 countries.
Funding
Abstract
Papillary thyroid cancer (PTC) is one of the most common endocrine malignancies associated with significant morbidity and mortality. Although multiple studies have contributed to a better understanding of the genetic alterations underlying this frequently arising disease, the downstream molecular effectors that impact PTC pathogenesis remain to be further defined. Here, we report that the regulator of cell fate specification, PROX1, becomes inactivated in PTC through mRNA downregulation and cytoplasmic mislocalization. Expression studies in clinical specimens revealed that aberrantly activated NOTCH signaling promoted PROX1 downregulation and that cytoplasmic mislocalization significantly altered PROX1 protein stability. Importantly, restoration of PROX1 activity in thyroid carcinoma cells revealed that PROX1 not only enhanced Wnt/β-catenin signaling but also regulated several genes known to be associated with PTC, including thyroid cancer protein (TC)-1, SERPINA1, and FABP4. Furthermore, PROX1 reexpression suppressed the malignant phenotypes of thyroid carcinoma cells, such as proliferation, motility, adhesion, invasion, anchorage-independent growth, and polyploidy. Moreover, animal xenograft studies demonstrated that restoration of PROX1 severely impeded tumor formation and suppressed the invasiveness and the nuclear/cytoplasmic ratio of PTC cells. Taken together, our findings demonstrate that NOTCH-induced PROX1 inactivation significantly promotes the malignant behavior of thyroid carcinoma and suggest that PROX1 reactivation may represent a potential therapeutic strategy to attenuate disease progression.
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