Key result
Ang1 induces PTC cell proliferation and migration by activating Tie2 and the PI3K/Akt pathway.
Why the study?
The role and mechanism of the Ang1/Tie2 pathway in the progression of papillary thyroid carcinoma remains unclear.
The Ang1/Tie2 pathway induces oncogenesis in papillary thyroid carcinoma via the PI3K/Akt pathway, suggesting a potential therapeutic target.
The angiopoietin 1 (Ang1)/angiopoietin receptor (Tie2) signaling pathway may have a notable role in the pathogenesis of inflammatory diseases. The abnormal expression of angiopoietin 1 and Tie2 has also been reported in various malignant tumors, including papillary thyroid carcinoma (PTC). However, the role and mechanism of the Ang1/Tie2 pathway in the progression of PTC remains unclear. Therefore, the aims of the present study were to clarify this. Significantly high expression levels of Ang1 and Tie2 were observed in PTC tissues and cell lines. Furthermore, MTT and wound-healing assays revealed that the Ang1-mediated stimulation of human PTC cells resulted in increased proliferation and migration. Conversely, the downregulation of Tie2 levels using short hairpin RNA targeted at Tie2 abrogated the Ang1-mediated effect on cell proliferation and migration. In studying the expression of phosphoinositide-3 kinase (PI3K)/RAC serine/threonine-protein kinase (Akt) pathway, the upregulation of Ang1/Tie2 was found to be associated with the activation of the PI3K/Akt pathway in PTC. In conclusion, the data from the present study indicated that the Ang1/Tie2 induces PTC oncogenesis via the PI3K/Akt pathway, providing novel insights into human PTC therapy.
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Ye et al. (2017) studied Papillary thyroid carcinoma (n=30). Ang1 overexpression and Tie2 knockdown vs. Control plasmids and adjacent normal tissues was evaluated on Cell proliferation and migration (p=<0.01). Ang1 and Tie2 are significantly upregulated in papillary thyroid carcinoma, and Ang1 induces PTC cell proliferation and migration by activating Tie2 and the PI3K/Akt pathway.
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