MiR-20b Displays Tumor-Suppressor Functions in Papillary Thyroid Carcinoma by Regulating the MAPK/ERK Signaling Pathway

Thyroid ◽  
2016 ◽  
Vol 26 (12) ◽  
pp. 1733-1743 ◽  
Author(s):  
Shubin Hong ◽  
Shuang Yu ◽  
Jin Li ◽  
Yali Yin ◽  
Yujie Liu ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Tumor Suppressor ◽  
Thyroid Carcinoma ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Papillary Thyroid

scholarly journals Depletion of VAX2 restrains the malignant progression of papillary thyroid carcinoma by modulating ERK signaling pathway

2019 ◽  
Vol 14 (1) ◽  
pp. 237-245
Author(s):  
Bei Guo ◽  
Yi Zhang ◽  
Kun Yuan ◽  
Feng-Xia Jiang ◽  
Qian-Bo Cui ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Western Blot ◽  
Signaling Pathway ◽  
Malignant Progression ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Erk Signaling ◽  
Migration And Invasion ◽  
Papillary Thyroid

AbstractObjectiveVentral anterior homeobox 2 (VAX2) gene is a key regulating factor for the development of the ventral region of the eye, and has recently attracted much attention from the cancer treatment field. Our study aimed to explore the effect of VAX2 on papillary thyroid carcinoma (PTC).MethodsWe determined the expression levels of VAX2 in PTC based on The Cancer Genome Atlas (TCGA) database. We then assessed the prognosis of patients with PTC, and analyzed the association between VAX2 expression and clinicopathological characteristics. Subsequently, we measured the biological functions of VAX2 in PTC using qRT-PCR, cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay, transwell assays and western blot.ResultsVAX2 was up-regulated in PTC tissues when compared with normal thyroid tissues, and high expression level of VAX2 was positively correlated with poor prognosis. Furthermore, knockdown of VAX2 significantly inhibited the proliferation, migration and invasion of PTC cells. Importantly, through western blot analysis, we found that the expression of phosphorylated-(p) ERK and p-MEK in ERK signaling pathway showed a significant decrease after knockdown of VAX2.ConclusionThese findings suggest that VAX2 may be involved in the malignant progression of PTC, and hold significant potential as a therapeutic target for PTC.

scholarly journals Tumor Suppressor LKB1 Inhibits Activation of Signal Transducer and Activator of Transcription 3 (STAT3) by Thyroid Oncogenic Tyrosine Kinase Rearranged in Transformation (RET)/Papillary Thyroid Carcinoma (PTC)

2007 ◽  
Vol 21 (12) ◽  
pp. 3039-3049 ◽  
Author(s):  
Dong Wook Kim ◽  
Hyo Kyun Chung ◽  
Ki Cheol Park ◽  
Jung Hwan Hwang ◽  
Young Suk Jo ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Tumor Suppressor ◽  
Thyroid Carcinoma ◽  
Malignant Tumors ◽  
Kinase Domain ◽  
Signal Transducer ◽  
Papillary Thyroid ◽  
Loss Of Function ◽  
Amino Acid Region ◽  
Transcription 3

Abstract The tumor suppressor LKB1 (STK11) is a cytoplasmic/nuclear serine/threonine kinase, defects in which cause Peutz-Jeghers syndrome (PJS) in humans and animals. Recent studies showed that loss of function of LKB1 is associated with sporadic forms of lung, pancreatic, and ovarian cancer. In cancer cells, LKB1 is inactivated by two mechanisms: mutations in its central kinase domain or complete loss of LKB1 expression. Inactivation of LKB1 is associated with progression of PJS and transformation of benign polyps into malignant tumors. This study examines the effect of LKB1 on regulation of STAT3 and expression of transcriptional targets of STAT3. The results show that LKB1 inhibits rearranged in transformation (RET)/papillary thyroid carcinoma (PTC)-dependent activation of signal transducer and activator of transcription 3 (STAT3), which is mediated by phosphorylation of STAT3 tyrosine 705 by RET/PTC. Suppression of STAT3 transactivation by LKB1 requires the kinase domain but not the kinase activity of LKB1. The centrally located kinase domain of LKB1 is an approximately 260-amino-acid region that binds to the linker domain of STAT3. Chromatin immunoprecipitation studies indicate that expression of LKB1 reduces the binding of STAT3 to its target promoters and suppresses STAT3-mediated expression of Cyclin D1, VEGF, and Bcl-xL. Knockdown of LKB1 by specific small interfering RNA led to an increase in STAT3 transactivation activity and promoted cell proliferation in the presence of RET/PTC. Thus, this study suggests that LKB1 suppresses tumor growth by inhibiting RET/PTC-dependent activation of oncogenic STAT3.

FoxP3 in papillary thyroid carcinoma induces NIS repression through activation of the TGF-β1/Smad signaling pathway

Tumor Biology ◽  
2015 ◽  
Vol 37 (1) ◽  
pp. 989-998 ◽  
Author(s):  
Siyuan Ma ◽  
Qingzhu Wang ◽  
Xiaojun Ma ◽  
Lina Wu ◽  
Feng Guo ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Signaling Pathway ◽  
Papillary Thyroid ◽  
Smad Signaling ◽  
Smad Signaling Pathway ◽  
Tgf Β1
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