Small molecule c-MET inhibitor PHA665752: Effect on cell growth and motility in papillary thyroid carcinoma

Head & Neck ◽  
2008 ◽  
Vol 30 (8) ◽  
pp. 991-1000 ◽  
Author(s):  
Chandrani Chattopadhyay ◽  
Adel K. El-Naggar ◽  
Michelle D. Williams ◽  
Gary L. Clayman
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Small Molecule ◽  
Papillary Thyroid ◽  
Met Inhibitor

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 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 LncRNA HOTAIR Influences the Growth, Migration, and Invasion of Papillary Thyroid Carcinoma via Affection on the miR-488-5p/NUP205 Axis

2020 ◽  
Vol 19 ◽  
pp. 153303382096212
Author(s):  
Feng Xia ◽  
Wei Xia ◽  
Xudong Yu
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
Well Assay ◽  
And Migration

Objective: The study was aim to investigate the effect of HOX transcript antisense RNA (HOTAIR) on the growth, migration, and invasion of papillary thyroid carcinoma (PTC) and its underlying mechanisms. Methods: Cell growth, invasion, and migration was respectively investigated using the MTT assay, trans-well assay, and wound healing assay. The expression of genes and proteins was respectively determined by Western blot analysis and RT-PCR experiments. Results: It was demonstrated that high expression of HOTAIR in PTC cells (BCPAP) and tissues resulted in fast tumor growth and poor survival time of the PTC-bearing mice models. Moreover, overexpression of HOTAIR leaded to markedly enhanced proliferation, migration, and invasion of BCPAP cells. Increase the levels of HOTAIR in BCPAP cells signally down-regulated the miR-488-5p levels which was able of inhibiting the growth rate, increasing the apoptosis rate, and decreasing the invasion/migration ability of BCPAP cells. Further studies indicated that HOTAIR promoted BCPAP cell growth, invasion, and migration mainly through regulating the miR-488-5p/NUP205 axis and the levels of Bcl-2 as well. Conclusion: HOTAIR promoted the growth, migration, and invasion of papillary thyroid carcinoma mainly through regulating the miR-488-5p/NUP205 axis.

miR-31 Reduces Cell Growth of Papillary Thyroid Carcinoma by RNA-Binding Protein HuR

2015 ◽  
Vol 61 (11/2015) ◽  
Author(s):  
Danping Wu ◽  
Bo Wang ◽  
Jiangfeng Shang ◽  
Jia Song ◽  
Hongdan Zhang
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Papillary Thyroid

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.

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