Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation

Thomasz, Lisa; Coulonval, Katia; Salvarredi, Leonardo; Oglio, Romina; Rossich, Luciano; Pisarev, Mario A.; Roger, Pierre P.; Juvenal, Guillermo

doi:10.1016/j.mce.2015.01.038

Cited by 7 publications

(3 citation statements)

References 42 publications

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“…Although thyroid gland function is mainly under pituitary TSH control [24], other factors such as miRNAs have significant roles in this process [25]. In contrast to miRNA, much less is known about lncRNA function in human cells, especially thyroid cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA BCAR4 up-regulates EGFR and thus promotes human thyrocyte proliferation

Zhai

Yan

Yang

et al. 2019

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This study establishes that BCAR4 has pro-proliferative effects on normal thyroid cells. BCAR4 up-regulation promotes proliferation and suppresses apoptosis of NTHY-ORI 3-1 cells and human primary thyrocytes, and EGFR is highly expressed in BCAR4 over-expressing-cells. In contrast, BCAR4 up-regulation did not modulate cell viability or cell cycle progression when EGFR was knocked-down. Further, the phosphorylated forms of PI3K, AKT, mTOR and p70S6K were up-regulated by BCAR4 up-regulation, and the alteration in these kinases induced by BCAR4 up-regulation was abolished when EGFR was knocked-down. This study therefore revealed the pro-proliferative role of lncRNA BCAR4 in NTHY-ORI 3-1 cells and human primary thyrocytes; where BCAR4 accelerated thyroid cells proliferation by EGFR up-regulation and the modulation of PI3K/AKT/mTOR signaling. These findings indicate that targeting BCAR4 has potential in hyperthyroidism treatment.

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Section: Discussionmentioning

confidence: 99%

LncRNA BCAR4 up-regulates EGFR and thus promotes human thyrocyte proliferation

Zhai

Yan

Yang

et al. 2019

neo

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“…Furthermore, IL-d has the goiter inhibitory activity due to the inhibition of cell proliferation and the transient stimulation of apoptosis. Interestingly, apoptosis in this case does not involve oxidative stress [38].…”

Section: Iodine Excess and Thyroid Cells Apoptosismentioning

confidence: 73%

Role of iodine in pathogenesis of thyroid disease - is induction of apoptosis consequence of iodine cytotoxicity?

Markovic¹

2017

Srp Arh Celok Lek

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Iodine is one of the best-characterized environmental factors associated with autoimmune thyroid disease (ATD). Epidemiological studies have shown that ATD incidence has increased following the introduction of salt iodination in the 1920s; in addition, ATD patients can improve upon iodine restriction. In animal models such as BioBreeding/Worcester and Buffalo rats, obese chicken strain, and non-obese diabetic H-2h4 mice, excess iodine is associated with autoimmunity. Analyses of Hashimoto thyroiditis (HT) have shown enlarged number of apoptotic follicular cells, and the destruction is an effect of death receptormediated apoptosis. Excess of iodine induces rapid apoptosis of goitrogen Wistar pretreated rats, possibly connected with inhibition of polyamine synthesis, inhibitors of DNA fragmentation. Percentage of apoptotic cells was statistically higher in patients with HT than in those with euthyroid goiter, with significant increase of caspase 32. Genes for Bcl-2 and Bax proteins are under the transcriptional control of p53. In TAD-2 cell cultures, apoptosis is p53-independed, suggesting that DNA damage is not primarily evoked by potassium iodide (KI). High concentrations of NaI increase the proportion of apoptotic cells in FTRL5 thyroid cell line. Iodide cytotoxicity is inhibited by a TPO inhibitor and is relieved with an anti-oxidant agent. Chronic iodine excess induces apoptosis and necrosis of thyroid follicular and endothelial cells, leading to thyroglobulin accumulation in connective tissue. Iodide excess requires peroxidase enzymatic activity to induce apoptosis. Ionic iodide is not directly toxic, whereas its molecular form I2 mediates the apoptotic effect of KI. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no. OI-175059]

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“…Our previous results have demonstrated that 2-IHDA has an antigoitrogenic activity, decreasing the intracellular levels of cAMP, thus reducing the number of cells and the glandular epithelial height (Thomasz et al, 2010a). Moreover 2-IHDA has an inhibitory effect on FRTL-5 thyroid cell proliferation mediated by cell cycle arrest and apoptosis (Thomasz et al, 2015).…”

Section: Discussionmentioning

confidence: 97%