Human Gene Set: MISIAK_ANAPLASTIC_THYROID_CARCINOMA_UP


Standard name MISIAK_ANAPLASTIC_THYROID_CARCINOMA_UP
Systematic name M45041
Brief description Genes up-regulated in anaplastic thyroid carcinoma and sharply distinguishing ATC from other thyroid carcinomas.
Full description or abstract Anaplastic thyroid carcinoma (ATC) is the most fatal and rapidly evolving endocrine malignancy invading the head and neck region and accounts for up to 50% of thyroid cancer-associated deaths. Deregulation of the microRNA (miRNA) expression promotes thyroid carcinoma progression by modulating the reorganization of the ATC transcriptome. Here, we applied comparative miRNA-mRNA sequencing on a cohort of 28 thyroid carcinomas to unravel the association of deregulated miRNA and mRNA expression. This identified 85 miRNAs significantly deregulated in ATC. By establishing a new analysis pipeline, we unraveled 85 prime miRNA-mRNA interactions supporting the downregulation of candidate tumor suppressors and the upregulation of bona fide oncogenes such as survivin (BIRC5) in ATC. This miRNA-dependent reprogramming of the ATC transcriptome provided an mRNA signature comprising 65 genes sharply distinguishing ATC from other thyroid carcinomas. The validation of the deregulated protein expression in an independent thyroid carcinoma cohort demonstrates that miRNA-dependent oncogenes comprised in this signature, the transferrin receptor TFRC (CD71) and the E3-ubiquitin ligase DTL, are sharply upregulated in ATC. This upregulation is sufficient to distinguish ATC even from poorly differentiated thyroid carcinomas (PDTC). In sum, these findings provide new diagnostic tools and a robust resource to explore the key miRNA-mRNA regulation underlying the progression of thyroid carcinoma.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 34885022   Authors: Misiak D,Bauer M,Lange J,Haase J,Braun J,Lorenz K,Wickenhauser C,Hüttelmaier S
Exact source Table S7: OncoScore ranked table of top-target mRNAs with best interactions
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Source species Homo sapiens
Contributed by Danny Misiak (Martin Luther University Halle-Wittenberg)
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Version history 2022.1.Hs: First Introduced.

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