scholarly journals MicroRNA-221 promotes papillary thyroid carcinoma cells migration and invasion via targeting RECK and regulating epithelial–mesenchymal transition

2019 ◽  
Vol Volume 12 ◽  
pp. 2323-2333 ◽  
Author(s):  
Zhao-li Wei ◽  
Ai-bin Gao ◽  
Qing Wang ◽  
Xiu-e Lou ◽  
Jing Zhao ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Mesenchymal Transition

scholarly journals CD73 Overexpression Promotes Progression and Recurrence of Papillary Thyroid Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3042 ◽  
Author(s):  
Young Mun Jeong ◽  
Haejin Cho ◽  
Tae-Min Kim ◽  
Yourha Kim ◽  
Sora Jeon ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
High Expression ◽  
Migration And Invasion ◽  
Recurrence Free Survival ◽  
Papillary Thyroid ◽  
Tumor Immune Escape ◽  
Free Survival ◽  
Mesenchymal Transition ◽  
Cd73 Expression

CD73 is involved in tumor immune escape and promotes the growth and progression of cancer cells. The functional role of CD73 expression in papillary thyroid carcinoma (PTC) has not yet been established. In 511 patients with PTC, immunohistochemistry for CD73 on tissue microarrays showed that the high expression of CD73 was associated with an aggressive histologic variant (p = 0.002), extrathyroidal extension (p < 0.001), lymph node metastasis (p < 0.001), and BRAFV600E mutation (p = 0.015). Survival analysis results showed that patients with high CD73 expression had worse recurrence-free survival (p = 0.023). CD73 inhibitors induced G1 cell cycle arrest and apoptosis, inhibited the migration and invasion of PTC cells, and suppressed tumor growth in PTC xenograft nude mice. High expression of CD73 (NT5E) mRNA was associated with unfavorable clinicopathologic characteristics, the abundance of Tregs and dendritic cells, depletion of natural killer (NK) cells, and high expression of immune checkpoint genes and epithelial-to-mesenchymal transition-related genes in The Cancer Genome Atlas (TCGA) dataset. Taken together, CD73 expression promotes tumor progression and predicts low recurrence-free survival. Targeting the CD73–adenosine axis in the tumor microenvironment offers an attractive pathway for therapeutic strategies aimed at advanced PTC.

scholarly journals Expression of heparanase regulates cell proliferation, apoptosis, migration and invasion in vitro in papillary thyroid carcinoma cells with multiple signaling pathways involved

2019 ◽  
Author(s):  
Chuanjia Yang ◽  
Siyang Zhang ◽  
Xiaoying Chang ◽  
Yonglian Huang ◽  
Dongxu Cui ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Signaling Pathways ◽  
Signaling Molecules ◽  
Carcinoma Cells ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Multiple Signaling

Abstract Background Heparanase (HPSE) is an endo-β-D-glucuronidase, which is found overexpressed in various human cancers. The purpose of our work was to investigate the possible role of HPSE and the involved signaling molecules in the development of papillary thyroid carcinoma. Methods In this study, the expression plasmid of HPSE and RNA interference with shRNA specific for HPSE were used to elucidate the effects of HPSE on proliferation, apoptosis, migration and invasion in papillary thyroid carcinoma cells of B-CPAP. The probable downstream signaling molecules of HPSE were also explored. Results The results showed that upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP cells, and interfered with cell apoptosis. On the contrary, knockdown of HPSE exhibited the opposite effects. Compared with the parental cells, HPSE silencing cells showed attenuated capabilities of proliferation, migration and invasion, yet the apoptotic rate of transfected cells was increased. The activations of various signaling molecules correlated with cell biological behavior were found to be regulated by HPSE upregulation or knockdown. Conclusions Our results suggested that HPSE probably contributed to the progression and metastasis of papillary thyroid carcinoma, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of papillary thyroid carcinoma.

scholarly journals LDHA induces EMT gene transcription and regulates autophagy to promote the metastasis and tumorigenesis of papillary thyroid carcinoma

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Xiukun Hou ◽  
Xianle Shi ◽  
Wei Zhang ◽  
Dapeng Li ◽  
Linfei Hu ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Glucose Metabolism ◽  
Thyroid Carcinoma ◽  
Therapeutic Target ◽  
Metabolic Reprogramming ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Mesenchymal Transition ◽  
Expression Levels

AbstractPapillary thyroid carcinoma (PTC) is one of the most common kinds of endocrine-related cancer and has a heterogeneous prognosis. Metabolic reprogramming is one of the hallmarks of cancers. Aberrant glucose metabolism is associated with malignant biological behavior. However, the functions and mechanisms of glucose metabolism genes in PTC are not fully understood. Thus, data from The Cancer Genome Atlas database were analyzed, and lactate dehydrogenase A (LDHA) was determined to be a potential novel diagnostic and therapeutic target for PTCs. The research objective was to investigate the expression of LDHA in PTCs and to explore the main functions and relative mechanisms of LDHA in PTCs. Higher expression levels of LDHA were found in PTC tissues than in normal thyroid tissues at both the mRNA and protein levels. Higher expression levels of LDHA were correlated with aggressive clinicopathological features and poor prognosis. Moreover, we found that LDHA not only promoted PTC migration and invasion but also enhanced tumor growth both in vitro and in vivo. In addition, we revealed that the metabolic products of LDHA catalyzed induced the epithelial–mesenchymal transition process by increasing the relative gene H3K27 acetylation. Moreover, LDHA knockdown activated the AMPK pathway and induced protective autophagy. An autophagy inhibitor significantly enhanced the antitumor effect of FX11. These results suggested that LDHA enhanced the cell metastasis and proliferation of PTCs and may therefore become a potential therapeutic target for PTCs.

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