ZNF703 is Overexpressed in Papillary Thyroid Carcinoma Tissues and Mediates K1 Cell Proliferation

2018 ◽  
Vol 26 (1) ◽  
pp. 355-364 ◽  
Author(s):  
Xiaolin Yang ◽  
Geling Liu ◽  
Luyang Zang ◽  
Ding Li ◽  
Fang Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Papillary Thyroid

scholarly journals Validation of MicroRNA-188-5p Inhibition Power on Tumor Cell Proliferation in Papillary Thyroid Carcinoma

2020 ◽  
Vol 29 ◽  
pp. 096368972091830 ◽  
Author(s):  
Ping Zhou ◽  
Andrew Irving ◽  
Huifang Wu ◽  
Juan Luo ◽  
Johana Aguirre ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Tumor Cell ◽  
Cellular Proliferation ◽  
Tumor Cell Proliferation ◽  
Papillary Thyroid ◽  
Tumor Tissues ◽  
Potential Biomarker ◽  
And Function

Given the crucial role of microRNAs in the cellular proliferation of various types of cancers, we aimed to analyze the expression and function of a cellular proliferation-associated miR-188-5p in papillary thyroid carcinoma (PTC). Here we demonstrate that miR-188-5p is downregulated in PTC tumor tissues compared with the associated noncancerous tissues. We also validate that the miR-188-5p overexpression suppressed the PTC cancer cell proliferation. In addition, fibroblast growth factor 5 (FGF5) is observed to be downregulated in the PTC tumor tissues compared with the associated noncancerous tissues. Subsequently, FGF5 is identified as the direct functional target of miR-188-5p. Moreover, the silencing of FGF5 was found to inhibit PTC cell proliferation, which is the same pattern as miR-188-5p overexpression. These results suggest that miR-188-5p-associated silencing of FGF5 inhibits tumor cell proliferation in PTC. It also highlights the importance of further evaluating miR-188-5p as a potential biomarker and therapy target in PTC.

scholarly journals MAPK and SHH pathways modulate type 3 deiodinase expression in papillary thyroid carcinoma

2016 ◽  
Vol 23 (3) ◽  
pp. 135-146 ◽  
Author(s):  
Mírian Romitti ◽  
Simone Magagnin Wajner ◽  
Lucieli Ceolin ◽  
Carla Vaz Ferreira ◽  
Rafaela Vanin Pinto Ribeiro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Phase Cell ◽  
Mrna Levels ◽  
Papillary Thyroid ◽  
Shh Pathway ◽  
Cycle Arrest ◽  
Type 3 ◽  
Sustained Activation

Type 3 deiodinase (DIO3, D3) is reactivated in human neoplasias. Increased D3 levels in papillary thyroid carcinoma (PTC) have been associated with tumor size and metastatic disease. The objective of this study is to investigate the signaling pathways involved inDIO3upregulation in PTC. Experiments were performed in human PTC cell lines (K1 and TPC-1 cells) or tumor samples.DIO3mRNA and activity were evaluated by real-time PCR and ion-exchange column chromatography respectively. Western blot analysis was used to determine the levels of D3 protein.DIO3gene silencing was performed via siRNA transfection.DIO3mRNA levels and activity were readily detected in K1 (BRAFV600E) and, at lower levels, in TPC-1 (RET/PTC1) cells (P<0.007 andP=0.02 respectively). Similarly,DIO3mRNA levels were higher in PTC samples harboring theBRAFV600Emutation as compared with those with RET/PTC1 rearrangement or negative for these mutations (P<0.001). Specific inhibition ofBRAFoncogene (PLX4032, 3 μM), MEK (U0126, 10–20 μM) or p38 (SB203580, 10–20 μM) signaling was associated with decreases inDIO3expression in K1 and TPC-1 cells. Additionally, the blockage of the sonic hedgehog (SHH) pathway by cyclopamine (10 μM) resulted in markedly decreases inDIO3mRNA levels. Interestingly, siRNA-mediatedDIO3silencing induced decreases on cyclin D1 expression and partial G1 phase cell cycle arrest, thereby downregulating cell proliferation. In conclusion, sustained activation of the MAPK and SHH pathways modulate the levels ofDIO3expression in PTC. Importantly,DIO3silencing was associated with decreases in cell proliferation, thus suggesting a D3 role in tumor growth and aggressiveness.

scholarly journals Overexpression of PAX8-AS1 Inhibits Malignant Phenotypes of Papillary Thyroid Carcinoma Cells via miR-96-5p/PKN2 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Ping Zhou ◽  
Tongdao Xu ◽  
Hao Hu ◽  
Fei Hua
Keyword(s):  
Cell Proliferation ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Luciferase Reporter ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Papillary Thyroid ◽  
Western Blot Assay ◽  
Proliferation And Apoptosis ◽  
Relationship Of

Background. Thyroid carcinoma (THCA) is the most frequent endocrine malignancy. Papillary thyroid carcinoma (PTC) is the major subtype of THCA, accounting for over 80% of all THCA cases. LncRNA PAX8-AS1, a tumor suppressor associated with various human cancers, has been reported to be relevant to the regulation of all sorts of cellular processes. The purpose of this study was to verify the role of PAX8-AS1 in PTC. Methods. Three human PTC cell lines (K1, TPC-1, and IHH4) and one normal human thyroid cell line, Nthy-ori3-1, were used in our study. The expression of genes was detected by qRT-PCR. The bioinformatic analysis and luciferase reporter assay were used to confirm the binding relationship of PAX8-AS1 to miR-96-5p, and the targeting relationship of miR-96-5p to PKN2 was also predicted. Cell proliferation and apoptosis capacities were assessed by MTT and flow cytometry, respectively. EdU assay was used to detect cell proliferation. Western blot assay was employed to examine protein expression. Results. The expression of PAX8-AS1 was decreased in PTC tissues and cells. PAX8-AS1 overexpression inhibited the proliferation of PTC cells and promoted cell apoptosis. In addition, PAX8-AS1 bonds with miR-96-5p, whose downregulation elevated the expression of PKN2 in PTC cells. Importantly, according to the rescue experiments, PKN2 silencing partially reversed the inhibitory effects of PAX8-AS1 expression on PTC cell proliferation and apoptosis. Conclusions. We found that the PAX8-AS1/miR-96-5p/PKN2 axis was closely related to the progression of PTC, which could be a potential target for treating PTC patients.

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

2020 ◽  
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 ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Downstream Signaling ◽  
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 (PTC). Methods The expression of HPSE was examined in 80 samples of PTC by immunohistochemistry. In cell studies, 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 PTC cells of B-CPAP and KTC-1. The probable downstream signaling molecules of HPSE were also explored. Results 75.0% (60 out of 80) of PTC samples was detected high expression of HPSE, which was significantly correlated with tumor size, lymph node metastasis and stage status. In cell studies, the upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP and KTC-1 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 PTC, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of PTC.

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