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Expression of Mitogen-Activated Protein Kinases in papillary Thyr | 6048
Journal of Thyroid Disorders & Therapy

Journal of Thyroid Disorders & Therapy
Open Access

ISSN: 2167-7948

+44 1300 500008

Expression of Mitogen-Activated Protein Kinases in papillary Thyroid carcinoma


International Conference on Thyroid Disorders and Treatment

February 29-March 01, 2016 Philadelphia, Pennsylvania, USA

Monika Lamba Saini

Universit�?© Catholique de Louvain, Belgium

Posters & Accepted Abstracts: Thyroid Disorders Ther

Abstract :

Papillary Thyroid carcinoma (PTC) is the most common endocrine malignancy, accounting for 85��?90% of all Thyroid cancers. PTC also frequently carries several alterations in genes coding for proteins that activate the Mitogen-activated protein kinases (MAPK) signalling pathway, which plays a key role in the regulation of cell growth and differentiation. This study aims to investigate the mitogen-activated protein kinase (MAPK) signaling pathway, [extracellular-regulated kinase (ERK), Jun N-terminal Kinase (JNK) and p38] involved in tumorigenesis of PTC. 20 samples of PTC were selected for immunohistochemical and Western blot analysis of total and phosphorylated ERK, JNK and p38. Effect of MAPK inhibitors U0126 (ERK inhibitor), SP 600125 (JNK inhibitor) and SB 203580 (p38 inhibitor) were analyzed on BC-PAP, TPC-1, and WR082-W-1 cell lines by MTT assay and Western blots. Phosphorylated p38 was seen as abundant nuclear and cytoplasmic immunolabelling in 11/20 cases, while ERK and JNK phosphorylation were seen in one and four cases respectively (p<0.01). By Western blotting, phosphorytated p38, phosphorylated ERK and JNK were detected in 17, 7 and 10 cases respectively.MTT assay showed a decrease in the number of viable cells in all the cell lines after culturing with the p38 and ERK inhibitor. Western blot analysis revealed decreased phosphorylation of p38 and ERK after treating with inhibitors. These data suggest that p38 is activated in a larger proportion of PTC than ERK or JNK. The molecular profiling of PTC could reveal the altered biological pathways involved in the genesis of this common endocrine malignancy.

Biography :

Email: monikalamba@gmail.com

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