| Grant number: | 14/50521-0 |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| Effective date (Start): | September 01, 2014 |
| Effective date (End): | August 31, 2018 |
| Field of knowledge: | Health Sciences - Medicine - Medical Clinics |
| Principal Investigator: | Edna Teruko Kimura |
| Grantee: | Cesar Seigi Fuziwara |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| Associated scholarship(s): | 17/01829-0 - Study the role of microRNA in cancer metastasis using genetically engineered mouse models, BE.EP.PD |
Abstract Genetic alterations in oncogenes and tumor supressor genes deregulate signaling pathways involved in proliferation, apoptosis and cell survival. Recently, microRNAs (miRNAs), small endogenous RNA that negatively regulate specific target mRNAs translation, have been implicated in oncogenesis, The expression of some miRNAs is associated to more aggressive cancers such as the cluster of miRNAs miR-17-92, detected in high levels in anaplastic thyroid cancer, the most aggressive of thyroid gland. Moreover, a certain fraction of papillary thyroid cancer shows miR-17-92 deregulation and aggressive behavior such as refractoriness to radioiodine therapy as anaplastic cells, being BRAF mutation a common feature in these cases. BRAFT1799A is the most frequent genetic alteration in thyroid cancer (2, 3) and induces miR-17-92 expression (4). Besides that, the knowledge of molecular activation/inhibition of miRNA transcription is not satisfactory. In silico studies show the presence of CpG islands in more than 50% of miRNA genes, indicating a potential epigenetic regulation. Therefore, in this project, we will study the molecular mechanisms involved in the transcription of miR-17-92 in thyroid cancer, investigating the role of epigenetic modifications such as methylation of CpG islands, modifications in histones of promoter region triggered by IncRNAs (long non-coding RNAs) and the role of transcription factors. Thus, we expect to contribute to the better understanding of molecular mechanism underlying transcription of miR-17-92 and its role in cancer progression, that would support the translational application of miRNA modulation in the treatment of patients with aggressive and refractory cancer. (AU) | |
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