MicroRNA-520a-3p suppresses epithelial-mesenchymal transition, invasion, and migration of papillary thyroid carcinoma cells via theJAK1-mediated JAK/STAT signaling pathway

2018 ◽  
Vol 234 (4) ◽  
pp. 4054-4067 ◽  
Author(s):  
Chang-Long Bi ◽  
Ying-Qi Zhang ◽  
Bo Li ◽  
Min Guo ◽  
Yi-Li Fu
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Papillary Thyroid ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Stat Signaling ◽  
And Migration

scholarly journals LncRNA PROX1-AS1 promotes proliferation, invasion, and migration in papillary thyroid carcinoma

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Yanyan Shen ◽  
Erjie Xia ◽  
Adheesh Bhandari ◽  
Xiaohui Wang ◽  
Guilong Guo
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Papillary Thyroid ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Tumorigenesis And Progression ◽  
And Migration ◽  
Thyroid Cancer Cell Lines

Evidence has been provided that long noncoding RNAs (LncRNAs) play major roles in affecting essential physiological processes, and many of which seem to have functional roles in tumorigenesis and progression. However, the intrinsic molecular mechanism of LncRNAs acting on papillary thyroid carcinoma is not well understood. In the present study, we found that PROX1-AS1 levels were obviously increased in thyroid cancer cells compared with the normal thyroid epithelial cells. Knockdown of PROX1-AS1 gene expression by siRNA could inhibit cell proliferation. Subsequently, we also observed that silencing PROX1-AS1 might inhibit invasion and migration of thyroid cancer cell lines via modulating the expression of epithelial–mesenchymal transition related proteins. In conclusion, our study indicated that LncRNA PROX1-AS1 could promote papillary thyroid carcinoma development and might serve as a potential targeting marker for papillary thyroid carcinoma.

The CXCL12–CXCR4 axis promotes migration, invasiveness, and EMT in human papillary thyroid carcinoma B-CPAP cells via NF-κB signaling

2018 ◽  
Vol 96 (5) ◽  
pp. 619-626 ◽  
Author(s):  
Yuanqiang Lin ◽  
Qingjie Ma ◽  
Lin Li ◽  
Hui Wang
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Papillary Thyroid ◽  
Mesenchymal Transition ◽  
Cxc Chemokine ◽  
Chemokine Ligand ◽  
Cxcr4 Axis

Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy involving local and distant metastasis. It is known that CXC chemokine ligand 12 (CXCL12) interacts specifically with CXC chemokine receptor 4 (CXCR4) to guide the migration of PTC cells. However, the signaling pathway downstream of the CXCL12–CXCR4 axis in PTC is not fully understood. In the present study, high expression of CXCR4 was detected in 38 out of 82 specimens of PTC, and the expression level of CXCR4 significantly correlated with the stage of PTC. Additionally, the roles of the CXCL12–CXCR4 axis in the migration, invasion, and epithelial–mesenchymal transition (EMT) of B-CPAP cells were investigated in vitro. The motility and invasiveness were significantly enhanced in CXCR4-overexpressing B-CPAP cells with CXCL12 treatment. Moreover, the CXCL12–CXCR4 axis promoted the EMT process, as evidenced by a decreased level of E-cadherin and increased expressions of N-cadherin and vimentin. Furthermore, the CXCL12–CXCR4 axis activated the nuclear factor kappa-B (NF-κB) signaling pathway, whereas BAY11-7082, an IκB phosphorylation inhibitor, counteracted CXCL12–CXCR4-induced migration, invasion, and EMT processes in B-CPAP cells. In conclusion, the CXCL12–CXCR4 axis promotes the migration, invasion, and EMT processes in B-CPAP cells, at least partly, by activating the NF-κB signaling pathway.

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