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Master's Dissertation
DOI
10.11606/D.42.2008.tde-09092008-163603
Document
Author
Full name
Ana Paula Zen Petisco Fiore
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2008
Supervisor
Committee
Kimura, Edna Teruko (President)
Cerutti, Janete Maria
Santelli, Glaucia Maria Machado
Title in Portuguese
Influência do excesso de iodo na ativação do oncogene RET/PTC3 na linhagem PCCL3 de tiróide de rato.
Keywords in Portuguese
Carcinoma papilífero
Cultura de células
Glândula tireóide
Iodo
Oncogenes
Via de sinalização MAPK
Abstract in Portuguese
Carcinomas papilíferos (CP) estão relacionados à ativação da via de sinalização MAPK por diversos oncogenes. Estudos têm relacionado a incidência de CP com a disponibilidade de iodo, um dos mais importante reguladores da função tiroidiana. Recentemente, nosso grupo descreveu que a inibição da via de sinalização TGFb pode estar vinculada ao desenvolvimento de CP. Nosso objetivo foi avaliar os efeitos do excesso de iodo na transformação de células tiroidianas. Utilizamos células PCCL3 com indução do oncogene RET/PTC3, tratadas com excesso de iodo. Observamos que o iodo reduziu a proliferação, sem alterar a morte das células e recuperou a expressão de genes específicos tiroidianos, evento geralmente vinculado à transformação maligna tiroidiana. O tratamento com excesso de iodo, ainda, reduziu a expressão de proteínas envolvidas na via MAPK e promoveu o restabelecimento da expressão da via TGFb, uma importante via inibitória da proliferação de células tiroidianas. Concluímos que o excesso iodo tenha uma ação antioncogênica durante a transformação maligna tiroidiana.
Title in English
Influence of iodine excess in RET/PTC3 oncogene activated PCCL3 thyroid cell lineage.
Keywords in English
Cell culture
Iodine
MAPK pathway
Oncogenes
Papillary carcinoma
Thyroid gland
Abstract in English
Papillary Carcinomas (PC) are frequently related to MAPK signaling pathway, activation by several oncogenes. Recent studies had related PC incidence and iodine availability, one of the most important thyroid function regulators. Our group has recently showed that TGFb pathway inhibition is directly related to PC development. Our aim was to evaluate iodine excess effects during thyroid cells transformation. We used the PCCL3 cells with RET/PTC3 oncogene induction, treated with iodine excess. We observed that iodine reduced the cell proliferation, not altering cell death and recovered thyroid specific genes expression, event frequently liked to thyroid cells malignant transformation. Iodine excess treatment also reduced MAPK proteins expression and reestablished TGFb pathway components expression, an important inhibitory pathway of epithelial cells. We can conclude that iodine excess treatment plays an antioncogenic role during thyroid malignant transformation.
 
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Publishing Date
2008-09-11
 
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