High Iodine Concentration Attenuates <i>RET/PTC3</i> Oncogene Activation in Thyroid Follicular Cells

Fiore, Ana Paula Zen Petisco; Fuziwara, César Seigi; Kimura, Edna Teruko

doi:10.1089/thy.2008.0408

Cited by 16 publications

(21 citation statements)

References 26 publications

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“…In an animal experimental study, Fiore et al. 42 reported that excess iodine acts as a protective factor in thyroid follicular cells during activation of RET/PTC3 and attenuates the tumorigenesis process. To the best of our knowledge, this study is the first study comparing the prevalence of RET/PTC rearrangements in thyroid carcinomas between iodine‐rich and iodine‐deficient countries.…”

Section: Discussionmentioning

confidence: 99%

Genetic alterations of differentiated thyroid carcinoma in iodine‐rich and iodine‐deficient countries

et al. 2016

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BRAF V600E mutation, RET rearrangements, and RAS mutations are the common genetic alterations in differentiated thyroid carcinomas derived from follicular thyroid cells. However, the relationship between these alterations and iodine intake is still controversial. To clarify the influence of iodine intake on the occurrence of differentiated thyroid carcinomas, we performed molecular analyses for two differentiated carcinomas, papillary thyroid carcinomas (PTCs) and follicular thyroid carcinomas (FTCs), from an iodine‐rich country (Japan) and an iodine‐deficient country (Vietnam). We examined 120 PTCs (67 Japanese and 53 Vietnamese) and 74 FTCs (51 Japanese and 23 Vietnamese). We carried out allele‐specific polymerase chain reaction (AS‐PCR) for BRAF V600E, PCR and direct sequencing for RAS mutations (codon 12, 13, and 61 in NRAS,HRAS, and KRAS), and RT‐PCR for RET/PTC1 and RET/PTC3. BRAF V600E was present in 55/67 (82.1%) Japanese PTCs and 44/53 (83%) Vietnamese PTCs. RET/PTC1 was identified in only one PTC from each country, and no samples had RET/PTC3. NRAS mutation was found in 17/51 (33.3%) Japanese FTCs and 4/23 (17.4%) Vietnamese FTCs. NRAS mutation was cited in codon 61 (20 cases) and codon 12 (one case). None of FTCs had KRAS or HRAS mutations. There were no significant differences in the prevalence of BRAF V600E,RET/PTC, or RAS mutations between the two countries. Our study showed no differences in genetic alterations of thyroid cancers from iodine‐rich and iodine‐deficient countries, possibly suggesting that iodine intake might not affect the genetic alterations of differentiated thyroid cancer.

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Section: Discussionmentioning

confidence: 99%

Genetic alterations of differentiated thyroid carcinoma in iodine‐rich and iodine‐deficient countries

et al. 2016

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“…Furthermore, iodine treatment attenuated the loss of NIS and TSHR gene and protein expression induced by Ret/Ptc3 oncogene induction. In addition, iodine treatment reduced RET and ERK phosphorylation, without altering BRAF and ERK expression, indicating an antioncogenic role for iodine excess during thyroid oncogenic activation (Fiore et al 2009). …”

Section: Iodine and Eating Habitsmentioning

confidence: 99%

The influence of the environment on the development of thyroid tumors: a new appraisal

Marcello¹,

Malandrino²,

Almeida³

et al. 2014

Endocrine Related Cancer

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Most epidemiological studies concerning differentiated thyroid cancers (DTC) indicate an increasing incidence over the last two decades. This increase might be partially explained by the better access to health services worldwide, but clinicopathological analyses do not fully support this hypothesis, indicating that there are carcinogenetic factors behind this noticeable increasing incidence. Although we have undoubtedly understood the biology and molecular pathways underlying thyroid carcinogenesis in a better way, we have made very little progresses in identifying a risk profile for DTC, and our knowledge of risk factors is very similar to what we knew 30-40 years ago. In addition to ionizing radiation exposure, the most documented and established risk factor for DTC, we also investigated the role of other factors, including eating habits, tobacco smoking, living in a volcanic area, xenobiotics, and viruses, which could be involved in thyroid carcinogenesis, thus, contributing to the increase in DTC incidence rates observed.

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“…Classicamente, é reconhecido que o excesso de iodo inibe a proliferação celular (Tramontano et al, 1989;Wolff et al, 1949) e RET/PTC3 na célula folicular tiroidiana in vitro, retardando seus efeitos deletérios como a instabilidade genômica e a perda de diferenciação, respectivamente (Fiore et al, 2008;Fuziwara et al, 2010). A suplementação de iodo pela ingestão de tabletes de iodeto de potássio (KI) é uma medida profilática recomendada pela Organização Mundial da Saúde (OMS) em caso de acidente nuclear para saturar a glândula com altas concentrações…”

Section: Lista De Ilustraçõesunclassified

“…e RET/PTC3 na célula folicular tiroidiana, retardando seus efeitos deletérios como a instabilidade genômica e a perda de diferenciação, respectivamente (Fiore et al, 2008;Fuziwara et al, 2010). Além disto, a alta dose de iodo reduz a viabilidade celular e induz apoptose de linhagens de câncer de tiroide .…”

Section: T1799aunclassified

“…A inibição seletiva de miR-19 e miR-17-5p resultou em efeito antiproliferativo pronunciado, e restaurou a expressão das proteínas PTEN e RB, respectivamente (Takakura et al, 2008 (Chakraborty et al, 2012;Chaulk et al, 2011) O pri-miRNA do cluster miR-17-92 se enovela em uma estrutura terciária globular que interfere no acesso da enzima DROSHA, sendo que os miRNAs que se localizam na periferia desta estrutura (miR-17, miR-19a e miR-20a) são mais facilmente processados em miRNAs maduros em relação aos que se encontram no núcleo da estrutura (miR-19b e miR-92a -17, miR-18, miR-19a, miR-19b e miR-20. Nosso grupo mostrou recentemente que o excesso de iodo exerce efeito protetor frente ativação do oncogene RET/PTC3 na célula folicular tiroidiana ao bloquear a fosforilação da quinase ERK (Fiore et al, 2009). Além disto, a alta dose de iodo também se mostrou protetora frente aos efeitos deletérios da instabilidade genômica causada pela ativação de BRAF T1799A (Fuziwara et al, 2010 (Fuziwara, Kimura, 2014).…”

Section: Efeito Do Bloqueio De Mir-19 Na Resposta Ao Tgfβunclassified

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O cluster de microRNAs miR-17-92 e seus alvos na oncogênese tiroidiana: influência de BRAFT1799A e de iodo.

Fuziwara¹

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High Iodine Concentration Attenuates RET/PTC3 Oncogene Activation in Thyroid Follicular Cells

Abstract: Our results indicate an antioncogenic role for excess iodine during thyroid oncogenic activation. These findings contribute to a better understanding of the effect of iodine on thyroid follicular cells, particularly how it may play a protective role during RET/PTC3 oncogene activation.

Cited by 16 publications

References 26 publications

Genetic alterations of differentiated thyroid carcinoma in iodine‐rich and iodine‐deficient countries

Genetic alterations of differentiated thyroid carcinoma in iodine‐rich and iodine‐deficient countries

The influence of the environment on the development of thyroid tumors: a new appraisal

O cluster de microRNAs miR-17-92 e seus alvos na oncogênese tiroidiana: influência de BRAFT1799A e de iodo.

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