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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

MicroRNA Deregulation in Anaplastic Thyroid Cancer Biology

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Autor(es):
Fuziwara, Cesar Seigi [1] ; Kimura, Edna Teruko [1]
Número total de Autores: 2
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Cell & Dev Biol, BR-05508000 Sao Paulo - Brazil
Número total de Afiliações: 1
Tipo de documento: Artigo de Revisão
Fonte: INTERNATIONAL JOURNAL OF ENDOCRINOLOGY; 2014.
Citações Web of Science: 37
Resumo

Anaplastic thyroid cancer (ATC) is among the most lethal types of cancers, characterized as a fast-growing and highly invasive thyroid tumor that is unresponsive to surgery and radioiodine, blunting therapeutic efficacy. Classically, genetic alterations in tumor suppressor TP53 are frequent, and cumulative alterations in different signaling pathways, such as MAPK and PI3K, are detected in ATC. Recently, deregulation in microRNAs (miRNAs), a class of small endogenous RNAs that regulate protein expression, has been implicated in tumorigenesis and cancer progression. Deregulation of miRNA expression is detected in thyroid cancer. Upregulation of miRNAs, such as miR-146b, miR-221, and miR-222, is observed in ATC and also in differentiated thyroid cancer (papillary and follicular), indicating that these miRNAs' overexpression is essential in maintaining tumorigenesis. However, specific miRNAs are downregulated in ATC, such as those of the miR-200 and miR-30 families, which are important negative regulators of cell migration, invasion, and epithelial-to-mesenchymal transition (EMT), processes that are overactivated in ATC. Therefore, molecular interference to restore the expression of tumor suppressor miRNAs, or to blunt overexpressed oncogenic miRNAs, is a promising therapeutic approach to ameliorate the treatment of ATC. In this review, we will explore the importance of miRNA deregulation for ATC cell biology. (AU)

Processo FAPESP: 10/51704-0 - O cluster de micrornas mir-17-92 e seus alvos na oncogenese tirouidiana: influencia de braft1799a e de iodo
Beneficiário:Cesar Seigi Fuziwara
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 11/50732-2 - Perfil de expressoes de micrornas na oncogenese tiroidiana: papel da regulacao pos-transcricional na progressao tumoral e influencia do iodo.
Beneficiário:Edna Teruko Kimura
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 13/11019-4 - Papel da nova família de proteínas tumor-específicas FAM83 no câncer de tiróide
Beneficiário:Edna Teruko Kimura
Linha de fomento: Auxílio à Pesquisa - Regular