scholarly journals LncRNA GAS8-AS1 suppresses papillary thyroid carcinoma cell growth through the miR-135b-5p/CCND2 axis

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
NingHeng Chen ◽  
DeTao Yin ◽  
Bing Lun ◽  
XueLi Guo
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Cell Cycle Progression ◽  
Gene Prediction ◽  
Tumor Formation ◽  
Cell Counting ◽  
Papillary Thyroid ◽  
Downstream Target

AbstractThe aim of the present study was to investigate the potential role of GAS8 antisense RNA 1 (GAS8-AS1) in papillary thyroid carcinoma (PTC). PcDNA3.1-GAS8-AS1 and si-GAS8-AS1, miR-135b-5p mimic and si-CCND2 were transfected into PTC cells. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8). QRT-PCR was used to determine expressions of GAS8-AS1, miR-135b-5p, and CCND2, and Western blot were detected protein level of CCND2. The miRNA target gene prediction site TargetScan was used to predict potential targets of GAS8-AS1 and miR-135b-5p. Cell cycle progression was analyzed by flow cytometry. We found that GAS8-AS1 was down-regulated in PTC cell lines and inhibited proliferation and cycle of PTC cell. GAS8-AS1 directly targets miR-135b-5p, and GAS8-AS1 could regulate a downstream target of miR-135b-5p, Cyclin G2 (CCNG2), in an miR-135b-5p-mediated manner. In addition, we also proved that overexpressed GAS8-AS1 inhibited tumor formation in vivo. GAS8-AS1 suppresses PTC cell growth through the miR-135b-5p/CCND2 axis.

scholarly journals The mTOR Kinase Inhibitor CZ415 Inhibits Human Papillary Thyroid Carcinoma Cell Growth

2018 ◽  
Vol 46 (2) ◽  
pp. 579-590 ◽  
Author(s):  
Xiaobin Li ◽  
Zongze Li ◽  
Yimin Song ◽  
Wenjing Liu ◽  
Ziwen Liu
Keyword(s):  
Cell Cycle ◽  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Kinase Inhibitor ◽  
Elisa Assay ◽  
Papillary Thyroid ◽  
Xenograft Tumor ◽  
Survival And Growth

Background/Aim: Mammalian target of rapamycin (mTOR) plays an important role in papillary thyroid carcinoma (PTC) cell progression. CZ415 is a novel, highly-efficient and specific mTOR kinase inhibitor. The current study tested the potential anti-tumor activity of CZ415 in human PTC cells. Methods: The established (TPC-1 cell line) and primary human PTC cells were treated with CZ415. Cell survival and growth were tested by Cell Counting Kit-8 assay and BrdU ELISA assay, respectively. Cell apoptosis was tested by caspase-3/-9 activity assay, Hoechst-33342 staining assay and single-stranded DNA ELISA assay. Cell cycle progression was tested by propidium iodide-FACS assay. The mTOR signaling was tested by Western blotting assay and co-immunoprecipitation assay. The mouse xenograft tumor model was applied to study the effect of CZ415 in vivo. Results: In cultured human PTC cells, treatment with CZ415 at nM concentrations significantly inhibited cell survival and growth. CZ415 induced apoptosis activation and cell cycle arrest in human PTC cells. CZ415 disrupted assembling of mTORC1 (mTOR-Raptor association) and mTORC2 (mTOR-Rictor-GβL association) in TPC-1 cells, which led to de-phosphorylation of the mTORC1 substrates (S6K1 and 4E-BP1) and the mTORC2 substrate AKT (Ser-473). Further studies show that the autophagy inhibitor 3-methyladenine (3-MA) or Beclin-1 shRNA aggravated CZ415-induced cytotoxicity against PTC cells. In vivo, CZ415 oral administration inhibited TPC-1 xenograft tumor growth in mice. Conclusion: Our results show that mTOR blockage by CZ415 inhibits PTC cell growth in vitro and in vivo.

circ_0005273 promotes thyroid carcinoma progression by SOX2 expression

2020 ◽  
Vol 27 (1) ◽  
pp. 11-21 ◽  
Author(s):  
Wei Zhang ◽  
Hang Zhang ◽  
Xudong Zhao
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Endocrine System ◽  
Tumor Promoter ◽  
Cell Counting ◽  
Circular Rnas ◽  
Papillary Thyroid ◽  
Sox2 Expression

Papillary thyroid carcinoma (PTC) is one of the most prevalent tumors in endocrine system. CircRNAs (circular RNAs) are widely known as critical regulators in tumorigenesis of papillary thyroid carcinoma (PTC). The present study focused on the functional investigation and potential molecular mechanism toward circ_0005273 in PTC progression. Gene Expression Omnibus datasets (GSE93522) and qRT-PCR (quantitative real-time PCR) analyses showed that circ_0005273 were upregulated in PTC tissues and cell lines. Moreover, circ_0005273 was located in the cytoplasm of PTC cells and suggested poor prognosis in PTC patients. In vivo and in vitro functional assays indicated that knockdown of circ_0005273 inhibited PTC tumor growth and progression, respectively. Mechanistically, miR-1183 was identified as functional target of circ_0005273, and circ_0005273 could directly bind to miR-1138 and relieve inhibition of SRY (sex-determining region Y)-box 2 (SOX2). Data from Cell Counting Kit-8, colony formation assays and transwell assays revealed that the oncogenic role of circ_0005273 on PTC progression dependent on miR-1183-mediated SOX2 expression. In conclusion, circ_0005273 functioned as a tumor promoter of PTC via circ_0005273/miR-1183/SOX2 axis, suggesting a novel biomarker and therapeutic target for PTC.

scholarly journals miR-622 suppresses tumor formation by directly targeting VEGFA in papillary thyroid carcinoma

2018 ◽  
Vol Volume 11 ◽  
pp. 1501-1509 ◽  
Author(s):  
Wang Renjie ◽  
Ma Qingjie ◽  
Ji Linlin ◽  
Yao Yue ◽  
Mengshi Ma ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Tumor Formation ◽  
Papillary Thyroid

scholarly journals CircLDLR Promotes Papillary Thyroid Carcinoma Tumorigenicity by Regulating miR-637/LMO4 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yuan-ming Jiang ◽  
Wei Liu ◽  
Ling Jiang ◽  
Hongbin Chang
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Papillary Thyroid ◽  
Induced Apoptosis

Background. Circular RNAs (circRNAs) have been reported to play important roles in the development and progression of papillary thyroid carcinoma (PTC). However, the function and molecular mechanism of circRNA low-density lipoprotein receptor (circLDLR) in the tumorigenesis of PTC remain unknown. Results. In this study, circLDLR was found to be markedly upregulated in PTC tissues and cell lines, and knockdown of circLDLR inhibited PTC cell proliferation, migration, and invasion but induced apoptosis in vitro. Moreover, circLDLR acted as a sponge for miR-637, and miR-637 interference reversed the anticancer effects of circLDLR knockdown on PTC cells. LMO4 was verified to be a target of miR-637; LMO4 upregulation abolished miR-637 mediated inhibition of cell growth and metastasis in PTC. Additionally, circLDLR could indirectly modulate LMO4 via acting as a sponge of miR-637 in PTC cells. Besides that, xenograft analysis showed that circLDLR knockdown suppressed tumor growth in vivo via regulating LMO4 and miR-637. Conclusion. Taken together, these results demonstrated that circLDLR promoted PTC tumorigenesis through miR-637/LMO4 axis, which may provide a novel insight into the understanding of PTC tumorigenesis and be useful in developing potential targets for PTC treatment.

scholarly journals Metformin reduces glycometabolism of papillary thyroid carcinoma in vitro and in vivo

2017 ◽  
Vol 58 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Chen-Tian Shen ◽  
Wei-Jun Wei ◽  
Zhong-Ling Qiu ◽  
Hong-Jun Song ◽  
Xin-Yun Zhang ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Xenograft Model ◽  
Dependent Manner ◽  
Papillary Thyroid ◽  
Fdg Uptake ◽  
Dose Dependent

More aggressive thyroid cancer cells show a higher activity of glycometabolism. Targeting cancer cell metabolism has emerged as a novel approach to prevent or treat malignant tumors. Glucose metabolism regulation effect of metformin in papillary thyroid cancer was investigated in the current study. Human papillary thyroid carcinoma (PTC) cell lines BCPAP and KTC1 were used. Cell viability was detected by CCK8 assay. Glucose uptake and relative gene expression were measured in metformin (0–10 mM for 48 h)-treated cells by 18F-FDG uptake assay and western blotting analysis, respectively. MicroPET/CT imaging was performed to detect 18F-FDG uptake in vivo. After treatment with metformin at 0, 2.5, 5 and 10 mM for 48 h, the ratio of p-AMPK to total AMPK showed significant rising in a dose-dependent manner in both BCPAP and KTC1, whereas p-AKT and p-mTOR expression level were downregulated. 18F-FDG uptake reduced after metformin treatment in a dose-dependent manner, corresponding to the reduced expression level of HK2 and GLUT1 in vitro. Xenograft model of PTC using BCPAP cells was achieved successfully. MicroPET/CT imaging showed that in vivo 18F-FDG uptake decreased after treatment with metformin. Immunohistochemistry staining further confirmed the reduction of HK2 and GLUT1 expression in the tumor tissue of metformin-treated PTC xenograft model. In conclusion, metformin could reduce glucose metabolism of PTC in vitro and in vivo. Metformin, by targeting glycometabolism of cancer cells, could be a promising adjuvant therapy alternative in the treatment modality of advanced thyroid carcinoma.

scholarly journals miR-219–5p Modulates Cell Growth of Papillary Thyroid Carcinoma by Targeting Estrogen Receptor α

2015 ◽  
Vol 100 (2) ◽  
pp. E204-E213 ◽  
Author(s):  
Chen Huang ◽  
Zhaogeng Cai ◽  
Mingzhu Huang ◽  
Chaoming Mao ◽  
Qifa Zhang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Estrogen Receptor Α ◽  
Papillary Thyroid

scholarly journals MEK Inhibitor PD0325901 Significantly Reduces the Growth of Papillary Thyroid Carcinoma Cells In vitro and In vivo

2010 ◽  
Vol 9 (7) ◽  
pp. 1968-1976 ◽  
Author(s):  
Ying C. Henderson ◽  
Yunyun Chen ◽  
Mitchell J. Frederick ◽  
Stephen Y. Lai ◽  
Gary L. Clayman
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Mek Inhibitor ◽  
Carcinoma Cells ◽  
Papillary Thyroid

scholarly journals A ceRNA network mediated by LINC00475 in papillary thyroid carcinoma

Open Medicine ◽  
2021 ◽  
Vol 17 (1) ◽  
pp. 22-33
Author(s):  
Yarong Yang ◽  
Wenjuan Hua ◽  
Mei Zeng ◽  
Liling Yu ◽  
Baijun Zhang ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Messenger Rna ◽  
Subcellular Fractionation ◽  
Suppressive Effect ◽  
Differentiated Thyroid Carcinoma ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Papillary Thyroid

Abstract Papillary thyroid carcinoma (PTC) is the most frequent histological type of differentiated thyroid carcinoma. Long noncoding RNAs (lncRNAs) have been widely reported to play a key role in human malignancies, and PTC is included. This study aimed to find out the functions and mechanism of lncRNA LINC00475 in PTC. LINC00475 was upregulated in PTC cells and was mainly located in the cytoplasm according to reverse-transcription polymerase chain reaction analyses and subcellular fractionation assays. As shown by cell counting kit-8 assays, ethynyl deoxyuridine incorporation assays, wound healing assays, and transwell assays, LINC00475 knockdown suppressed cell viability, proliferation, migration, and invasion. Mechanistically, LINC00475 upregulated the expression of messenger RNA zinc finger CCHC-type containing 12 (ZCCHC12) by binding to miR-376c-3p. ZCCHC12 was a direct target gene of miR-376c-3p in PTC cells. The relationship between miR-376c-3p and LINC00475 (or ZCCHC12) in PTC cells was probed by luciferase reporter assays, RNA pulldown assays, and RNA immunoprecipitation assays. In addition, both mRNA and protein levels of ZCCHC12 were downregulated due to miR-376c-3p overexpression or LINC00475 silencing. ZCCHC12 overexpression partially reversed the suppressive effect of LINC00475 knockdown on malignant behaviors of PTC cells. In conclusion, LINC00475 promotes PTC cell proliferation, migration, and invasion by upregulating ZCCHC12 via the interaction with miR-376c-3p.

scholarly journals HOOK3-RET: a novel type of RET/PTC rearrangement in papillary thyroid carcinoma

2007 ◽  
Vol 14 (2) ◽  
pp. 445-452 ◽  
Author(s):  
Raffaele Ciampi ◽  
Thomas J Giordano ◽  
Kathryn Wikenheiser-Brokamp ◽  
Ronald J Koenig ◽  
Yuri E Nikiforov
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Homo Sapiens ◽  
Functional Characterization ◽  
Coiled Coil ◽  
Gene Expression Signature ◽  
Tumor Formation ◽  
Fusion Product ◽  
Papillary Thyroid ◽  
Nih3t3 Cells

Chromosomal rearrangements of the RET proto-oncogene (RET/PTC) are the common feature of papillary thyroid carcinoma (PTC). In this study, we report the identification, cloning, and functional characterization of a novel type of RET/PTC rearrangement that results from the fusion of the 3′-portion of RET coding for the tyrosine kinase (TK) domain of the receptor to the 5′-portion of the Homo sapiens hook homolog 3 (HOOK3) gene. The novel fusion was identified in a case of PTC that revealed a gene expression signature characteristic of RET/PTC on DNA microarray analysis, but was negative for the most common types of RET rearrangement. A fusion product between exon 11 of HOOK3 and exon 12 of RET gene was identified by 5′RACE, and the presence of chimeric HOOK3-RET protein of 88 kDa was detected by western blot analysis with an anti-RET antibody. The protein is predicted to contain a portion of the coiled-coil domains of HOOK3 and the intact TK domain of RET. Expression of the HOOK3-RET cDNA in NIH3T3 cells resulted in the formation of transformed foci and in tumor formation after injection into nude mice, confirming the oncogenic nature of HOOK3-RET.

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