Genome-wide expression analysis suggests a crucial role of dysregulation of matrix metalloproteinases pathway in undifferentiated thyroid carcinoma |
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Authors: | Jesús Espinal-Enríquez Said Mu?oz-Montero Ivan Imaz-Rosshandler Aldo Huerta-Verde Carmen Mejía Enrique Hernández-Lemus |
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Affiliation: | .National Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610 México ;.Center for Sciences of Complexity (C3), UNAM, Ciudad Universitaria, México City, 01010 México ;.Faculty of Natural Sciences, Autonomous University of Querétaro, P.O. Box 184, Querétaro, 76230 México |
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Abstract: | BackgroundThyroid cancer (TC) is the most common malignant cancer of the Endocrine System. Histologically, there are three main subtypes of TC: follicular, papillary and anaplastic. Diagnosing a thyroid tumor subtype with a high level of accuracy and confidence is still a difficult task because genetic, molecular and cellular mechanisms underlying the transition from differentiated to undifferentiated thyroid tumors are not well understood.A genome-wide analysis of these three subtypes of thyroid carcinoma was carried out in order to identify significant differences in expression levels as well as enriched pathways for non-shared molecular and cellular features between subtypes.ResultsInhibition of matrix metalloproteinases pathway is a major event involved in thyroid cancer progression and its dysregulation may result crucial for invasiveness, migration and metastasis. This pathway is drastically altered in ATC while in FTC and PTC, the most important pathways are related to DNA-repair activation or cell to cell signaling events.ConclusionA progression from FTC to PTC and then to ATC was detected and validated on two independent datasets. Moreover, PTX3, COLEC12 and PDGFRA genes were found as possible candidates for biomarkers of ATC while GPR110 could be tested to distinguish PTC over other tumor subtypes. The genome-wide analysis emphasizes the preponderance of pathway-dysregulation mechanisms over simple gene-malfunction as the main mechanism involved in the development of a cancer phenotype.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1372-0) contains supplementary material, which is available to authorized users. |
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Keywords: | Anaplastic thyroid cancer Inhibition of matrix metalloproteinases Pathway analysis Thyroid carcinoma progression Genome-wide analysis |
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