scholarly journals MicroRNA deregulation in human thyroid papillary carcinomas

2006 ◽  
Vol 13 (2) ◽  
pp. 497-508 ◽  
Author(s):  
P Pallante ◽  
R Visone ◽  
M Ferracin ◽  
A Ferraro ◽  
M T Berlingieri ◽  
...  
Keyword(s):  
Cell Lines ◽  
Expression Profile ◽  
Mirna Expression ◽  
Mirna Expression Profile ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Rt Pcr ◽  
Normal Thyroid ◽  
Thyroid Papillary ◽  
Rat Thyroid

MicroRNAs (miRNAs) are a class of small non-coding RNAs involved in a wide range of basic processes such as cell proliferation, development, apoptosis and stress response. It has recently been found that they are also abnormally expressed in many types of human cancer. We analyzed the genome-wide miRNA expression profile in human thyroid papillary carcinomas (PTCs) using a microarray (miRNACHIP microarray) containing hundreds of human precursor and mature miRNA oligonucleotide probes. Using this approach, we found an aberrant miRNA expression profile that clearly differentiates PTCs from normal thyroid tissues. In particular, a significant increase in miRNA (miR)-221, -222 and -181b was detected in PTCs in comparison with normal thyroid tissue. These results were further confirmed by northern blot and quantitative RT-PCR analyses. Moreover, RT-PCR revealed miR-221, -222 and -181b overexpression in fine needle aspiration biopsies corresponding to thyroid nodules, which were eventually diagnosed as papillary carcinomas after surgery. Finally, miR-221, -222 and -181b overexpression was also demonstrated in transformed rat thyroid cell lines and in mouse models of thyroid carcinogenesis. Functional studies, performed by blocking miR-221 function and by overexpressing miR-221 in human PTC-derived cell lines, suggest a critical role of miR-221 overexpression in thyroid carcinogenesis. In conclusion, these data, taken together, indicate an miRNA signature associated with PTCs, and suggest miRNA deregulation as an important event in thyroid cell transformation.

scholarly journals Trace Amine-Associated Receptor 1 Trafficking to Cilia of Thyroid Epithelial Cells

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1518
Author(s):  
Maria Qatato ◽  
Vaishnavi Venugopalan ◽  
Alaa Al-Hashimi ◽  
Maren Rehders ◽  
Aaron D. Valentine ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cell Lines ◽  
Human Thyroid ◽  
Apical Plasma Membrane ◽  
Thyroid Cell ◽  
Thyroid Cells ◽  
Trace Amine ◽  
Rat Thyroid

Trace amine-associated receptor 1 (rodent Taar1/human TAAR1) is a G protein-coupled receptor that is mainly recognized for its functions in neuromodulation. Previous in vitro studies suggested that Taar1 may signal from intracellular compartments. However, we have shown Taar1 to localize apically and on ciliary extensions in rodent thyrocytes, suggesting that at least in the thyroid, Taar1 may signal from the cilia at the apical plasma membrane domain of thyrocytes in situ, where it is exposed to the content of the follicle lumen containing putative Taar1 ligands. This study was designed to explore mouse Taar1 (mTaar1) trafficking, heterologously expressed in human and rat thyroid cell lines in order to establish an in vitro system in which Taar1 signaling from the cell surface can be studied in future. The results showed that chimeric mTaar1-EGFP traffics to the apical cell surface and localizes particularly to spherical structures of polarized thyroid cells, procilia, and primary cilia upon serum-starvation. Moreover, mTaar1-EGFP appears to form high molecular mass forms, possibly homodimers and tetramers, in stably expressing human thyroid cell lines. However, only monomeric mTaar1-EGFP was cell surface biotinylated in polarized human thyrocytes. In polarized rat thyrocytes, mTaar1-EGFP is retained in the endoplasmic reticulum, while cilia were reached by mTaar1-EGFP transiently co-expressed in combination with an HA-tagged construct of the related mTaar5. We conclude that Taar1 trafficking to cilia depends on their integrity. The results further suggest that an in vitro cell model was established that recapitulates Taar1 trafficking in thyrocytes in situ, in principle, and will enable studying Taar1 signaling in future, thus extending our general understanding of its potential significance for thyroid autoregulation.

scholarly journals Hodgkin Lymphoma Cell Lines Are Characterized by a Specific miRNA Expression Profile

Neoplasia ◽  
2009 ◽  
Vol 11 (2) ◽  
pp. 167-IN9 ◽  
Author(s):  
Johan H. Gibcus ◽  
Lu Ping Tan ◽  
Geert Harms ◽  
Rikst Nynke Schakel ◽  
Debora de Jong ◽  
...  
Keyword(s):  
Hodgkin Lymphoma ◽  
Cell Lines ◽  
Expression Profile ◽  
Mirna Expression ◽  
Mirna Expression Profile ◽  
Lymphoma Cell ◽  
Hodgkin Lymphoma Cell

scholarly journals Increased P2X7 Receptor Expression and Function in Thyroid Papillary Cancer: A New Potential Marker of the Disease?

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 389-396 ◽  
Author(s):  
Anna Solini ◽  
Sabina Cuccato ◽  
Davide Ferrari ◽  
Eleonora Santini ◽  
Sara Gulinelli ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Cell Lines ◽  
P2x7 Receptor ◽  
Receptor Expression ◽  
Human Thyroid ◽  
Cytokine Release ◽  
Papillary Cancer ◽  
Normal Thyroid ◽  
Thyroid Papillary

Nucleotides are increasingly recognized as nonredundant extracellular signals for chemotaxis, cell growth, and cytokine release. Effects of extracellular nucleotides are mediated by P2 receptors, among which the P2X7 subtype is attracting increasing attention for its involvement in apoptosis, cell growth, and cytokine release. Recent studies showed that P2X7 is overexpressed in chronic lymphocytic leukemia and breast and prostate cancer. The aim of the present study was to better understand the clinical significance of P2X7 receptor expression in normal and cancer human thyroid tissues. P2X7 receptor message and protein expression and functional activity were tested in two cell lines (FB1 and FB2) established from either anaplastic or papillary primary thyroid cancer and in several histological samples of human papillary cancer. We show here that human thyroid papillary carcinoma, whether of the classical or follicular variant, expresses the P2X7 receptor (P2X7R) to a much higher level than normal thyroid tissue. The P2X7R was similarly up-regulated in FB1 and FB2 cell lines. In contrast to normal thyroid cells, both cell lines responded to extracellular nucleotide stimulation with a large increase in intracellular Ca2+ and secretion of IL-6. Ca2+ increase was attenuated and release of IL-6 was fully blocked by P2X7R inhibitors. Finally, the thyroid carcinoma cell lines had at least a 3-fold higher intracellular ATP concentration and maintained at least a 3-fold higher extracellular ATP level, compared with control cells. These data suggest that an enhanced P2X7R function might be a feature of human thyroid cancer.

scholarly journals EGF and TGF-1 Effects on Thyroid Function

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Gabriella Mincione ◽  
Maria Carmela Di Marcantonio ◽  
Chiara Tarantelli ◽  
Sonia D'Inzeo ◽  
Arianna Nicolussi ◽  
...  
Keyword(s):  
Growth Factors ◽  
Cell Lines ◽  
Cross Talk ◽  
Early Stage ◽  
Tumor Promoter ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Thyroid Tumors ◽  
Thyroid Cells ◽  
Rat Thyroid

Normal epithelial thyroid cells in culture are inhibited by TGF-1. Instead, transformed thyroid cell lines are frequently resistant to its growth inhibitory effect. Loss of TGF- responsiveness could be due to a reduced expression of TGF- receptors, as shown in transformed rat thyroid cell lines and in human thyroid tumors, or to alterations of other genes controlling TGF- signal transduction pathway. However, in thyroid neoplasia, a complex pattern of alterations occurring during transformation and progression has been identified. Functionally, TGF-1 acts as a tumor suppressor in the early stage of transformation or as a tumor promoter in advanced cancer. This peculiar pleiotropic behaviour of TGF- may result from cross-talk with signalling pathways mediated by other growth factors, among which EGF-like ligands play an important role. This paper reports evidences on TGF-1 and EGF systems in thyroid tumors and on the cross-talk between these growth factors in thyroid cancer.

scholarly journals Serial Analysis of Gene Expression as a Tool to Assess the Human Thyroid Expression Profile and to Identify Novel Thyroidal Genes*

2000 ◽  
Vol 85 (5) ◽  
pp. 1923-1927
Author(s):  
E. Pauws ◽  
J. C. Moreno ◽  
M. Tijssen ◽  
F. Baas ◽  
J. J. M. de Vijlder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profile ◽  
Messenger Rna ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Novel Genes ◽  
Normal Thyroid ◽  
Thyroid Neoplasia ◽  
Normal Human

Abstract The assessment of the expression profile of normal human thyroid tissue using serial analysis of gene expression (SAGE) generated a collection of 10,994 sequence transcripts (tags). Each tag represented a messenger RNA transcript, and, in total, 6099 different tags could be distinguished. The presence and abundance of thyroid-specific transcripts showed the overall expression profile to be from a normal thyroid cell. The expression level of several transcripts was confirmed on Northern blot. Seventy percent of tags could not be attributed to a known human gene and, therefore, possibly correspond to novel genes putatively involved in thyroid function. The tag sequence generated by the SAGE technique can be used to further characterize these novel genes. In this way, application of the SAGE technique to thyroid tissue gives insight in the expression profile of a normal thyroid gland and provides the information to characterize novel genes involved in thyroid pathology, such as congenital hypothyroidism and thyroid neoplasia.

Abstract WP319: miRNA Screening of Natural Killer Cell Identifies miR-1224 as a Post-Transcriptional Regulator of NK Cell Function After Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yan Feng ◽  
Hui Zhao ◽  
Fu-Dong Shi ◽  
Weina Jin
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Nk Cells ◽  
Expression Profile ◽  
Mirna Expression ◽  
Cell Function ◽  
Nk Cell ◽  
Killer Cell ◽  
Mirna Expression Profile ◽  
Control Group

Objectives: To screen miRNA profile of peripheral NK cells in ischemic stroke mouse model and investigate a most promising candidate (miR-1224) for post-transcriptional regulation of NK cell function after ischemic stroke. Methods: Mice were subjected to a 60 min focal cerebral ischemia produced by transient intraluminal occlusion of MCAO. For NK cell isolation, cell suspensions from the spleens after reperfusion were enriched for NK cells using magnetic-bead sorting system after staining with anti-NK1.1 microbeads. The nCounter Mouse miRNA array was used to analyze miRNA expression profile in splenic NK cells over the time course of experimental ischemic stroke. Based on the miRNA data, we further in vitro modulated miR-1224 in NK cells using mimics or inhibitor, then injected i.v into Rag2-/-γc-/- recipient mice. Neurological function score was compared and spontaneous infection was assessed by pulmonary bacteria colony culture, and changes in potential signaling pathway (SP1/TNF-α) were verified by rt-PCR and western blot. Results: Through miRNA expression profile analysis, we have identified significant changes at each time point in peripheral NK cells after cerebral ischemia. Among all screened miRNA, miR-1224 remarkably increased in MCAO group, which was verified by PCR. Then isolated NK cells treated with mimics or inhibitors, were transferred to Rag2-/-γc-/- recipient mice. Compared with WT mice, Rag2-/-γc-/- mice with miR-1224 inhibitor exhibited increased NK cell number, enhanced NK cell activation/cytotoxicity feature, as well as better neurological behaviors and reduced pulmonary infection after MCAO. Moreover, compared with the control group, NK cells with miR-1224 inhibitor showed significantly increased SP1 gene and protein phosphorylation. As SP1 gene is one of the potential targets of miR-1224, this study suggests that miR-1224 may regulate NK cell function after MCAO, which is associated with SP1 pathway. Conclusion: The miRNA profiling of splenic NK cells provided insight into the functional mechanism and signaling pathways underlying the distinct organ-specific NK cell properties, which will contribute to the better understanding of NK cell mediated immune-response in relation to different stages of stroke.

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