MiR-144-3p promotes the tumor growth and metastasis of papillary thyroid carcinoma by targeting paired box gene 8.
MiR-144-3p promotes the tumor growth and metastasis of papillary thyroid carcinoma by targeting paired box gene 8.
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DOI:
10.1186/s12935-018-0550-y
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发表时间:
2018
影响因子:
5.8
通讯作者:
Li G
中科院分区:
文献类型:
--
作者:
Liu C;Su C;Chen Y;Li G
Paired box gene 8 (PAX8) is expressed in and indispensable to thyroid development. MiR-144-3p is found dys-regulated in cancers, and it can block the expression of target gens. This study sought to understand the effect of MiR-144-3p in papillary thyroid carcinoma (PTC) as well as the associated mechanisms. Real-time PCR, immunohistochemical and Western blot assays were performed to examine the expression of target miRNA and/or genes. CCK-8 and flow cytometry analysis was used to respectively test cell growth, cell cycle progression and apoptosis. Luciferase reporter assay was performed to find out whether miR-144-3p could bind to the 3′ untranslated region of PAX8 or not. We found that PAX8 decreased in PTC, while miR-144-3p increased in PTC. Over-expression of miR-144-3p promoted the cell viability and cell cycle progression. The expressions of cell-cycle-related genes, cyclin D1, cyclin-dependent kinase 2 and CDC25A were modulated by miR-144-3p. Meanwhile, the presence or absence of miR-144-3p both affected epithelial-mesenchymal transition of PTC by regulating the expression of E-cadherin, N-cadherin and vimentin. Moreover, PAX8 may be a potential direct target of miR-144-3p. Mechanically, the activation of extracellular signal–regulated kinases 1/2, Akt and c-Jun N-terminal kinases may be associated with the tumor-promoting effect of miR-144-3p. In addition, the blockage of miR-144-3p forced the anti-tumor effect delivered by X-ray exposure or paclitaxel. MiR-144-3p promoted the growth of tumor and the metastasis of PTC by targeting PAX 8. The study provided promising prognosis markers and valuable treatment strategy for PTC.
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影响因子:
4.6
作者:
Nasu Y;Benke A;Arakawa S;Yoshida GJ;Kawamura G;Manley S;Shimizu S;Ozawa T
通讯作者:
Ozawa T
影响因子:
2.9
作者:
Katayama, Yuki;Maeda, Moegi;Tanaka, Hiroshi
通讯作者:
Tanaka, Hiroshi
影响因子:
7.5
作者:
Nonaka, Daisuke;Tang, Yunjia;Ghossein, Ronald
通讯作者:
Ghossein, Ronald
影响因子:
--
作者:
Carvalheira G;Nozima BH;Cerutti JM
通讯作者:
Cerutti JM
DOI:
10.1186/s13046-014-0105-6
发表时间:
2014-12-14
期刊:
Journal of experimental & clinical cancer research : CR
影响因子:
--
作者:
Du R;Wu S;Lv X;Fang H;Wu S;Kang J
通讯作者:
Kang J