ArticleCancer biology & therapy2016
EDAG-1 promotes proliferation and invasion of human thyroid cancer cells by activating MAPK/Erk and AKT signal pathways.
Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024Article
- Hemogen/BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis.Blood · 2022Article
- ANGPTL1 is a potential biomarker for differentiated thyroid cancer diagnosis and recurrence.Oncology letters · 2020Article
- Anti-Remodeling Effects of Xanthohumol-Fortified Beer in Pulmonary Arterial Hypertension Mediated by ERK and AKT Inhibition.Nutrients · 2019Article
- Up-regulation of CKAP2L expression promotes lung adenocarcinoma invasion and is associated with poor prognosis.OncoTargets and therapy · 2019Article
- DivergentBiology open · 2018Article
- Verteporfin inhibits papillary thyroid cancer cells proliferation and cell cycle through ERK1/2 signaling pathway.Journal of Cancer · 2018Article
- Yes-associated protein 1 promotes papillary thyroid cancer cell proliferation by activating the ERK/MAPK signaling pathway.Oncotarget · 2017Article
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Authors and funding
9 authors.
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Abstract
Erythroid differentiation-associated gene (EDAG) is differentially expressed in normal hematopoietic progenitor/stem cells and a variety of embryonic tissues. High EDAG-1 expression is also found in human thyroid cancer cells and peripheral blood of patients with leukemia, but its functional significance was unclear. Current study aims to further clarify the expression pattern of EDAG-1 and tests its roles in proliferation and invasion of human thyroid cancer cells in vitro and in vivo. To this end, we have performed gain-of-function and loss-of-function studies to clarify how EDAG-1 regulates the proliferation, invasion, and adhesion ability of human thyroid cancer cells SW579cells. We found that overexpression of EDAG-1 promoted the proliferation, invasion, and adhesion of human thyroid cancer cells, whereas silencing of EDAG-1 reversed all these changes and reduced the tumorigenesis risk of nude mice. Mechanistically, we found that overexpression of EDAG-1 activated the MAPK/Erk and AKT signal pathways. These findings provide novel insights of the role of EDAG-1 in thyroid tumors, and may have direct clinical implication.
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