scholarly journals Correction: miR-451a is underexpressed and targets AKT/mTOR pathway in papillary thyroid carcinoma

Oncotarget ◽  
2018 ◽  
Vol 9 (15) ◽  
pp. 12534-12534 ◽  
Author(s):  
Emanuela Minna ◽  
Paola Romeo ◽  
Matteo Dugo ◽  
Loris De Cecco ◽  
Katia Todoerti ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Mtor Pathway ◽  
Papillary Thyroid

scholarly journals miR-451a is underexpressed and targets AKT/mTOR pathway in papillary thyroid carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (11) ◽  
pp. 12731-12747 ◽  
Author(s):  
Emanuela Minna ◽  
Paola Romeo ◽  
Matteo Dugo ◽  
Loris De Cecco ◽  
Katia Todoerti ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Mtor Pathway ◽  
Papillary Thyroid

scholarly journals mTOR Pathway in Papillary Thyroid Carcinoma: Different Contributions of mTORC1 and mTORC2 Complexes for Tumor Behavior and SLC5A5 mRNA Expression

2018 ◽  
Vol 19 (5) ◽  
pp. 1448 ◽  
Author(s):  
Catarina Tavares ◽  
Catarina Eloy ◽  
Miguel Melo ◽  
Adriana Gaspar da Rocha ◽  
Ana Pestana ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Mrna Expression ◽  
Mtor Pathway ◽  
Papillary Thyroid

scholarly journals mTOR Pathway Overactivation in BRAF Mutated Papillary Thyroid Carcinoma

2012 ◽  
Vol 97 (7) ◽  
pp. E1139-E1149 ◽  
Author(s):  
Alexandra Faustino ◽  
Joana P. Couto ◽  
Helena Pópulo ◽  
Ana Sofia Rocha ◽  
Fernando Pardal ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Genetic Alterations ◽  
Mtor Pathway ◽  
Expression Vectors ◽  
Papillary Thyroid ◽  
Brafv600e Mutation ◽  
Pathway Activation

Abstract Context: There are several genetic and molecular evidences suggesting dysregulation of the mammalian target of rapamycin (mTOR) pathway in thyroid neoplasia. Activation of the phosphatidylinositol-3-kinase/AKT pathway by RET/PTC and mutant RAS has already been demonstrated, but no data have been reported for the BRAFV600E mutation. Objective: The aim of this study was to evaluate the activation pattern of the mTOR pathway in malignant thyroid lesions and whether it may be correlated with known genetic alterations, as well as to explore the mechanisms underlying mTOR pathway activation in these neoplasias. Results: We observed, by immunohistochemical evaluation, an up-regulation/activation of the mTOR pathway proteins in thyroid cancer, particularly in conventional papillary thyroid carcinoma (cPTC). Overactivation of the mTOR signaling was particularly evident in cPTC samples harboring the BRAFV600E mutation. Transfection assays with BRAF expression vectors as well as BRAF knockdown by small interfering RNA revealed a positive association between BRAF expression and mTOR pathway activation, which appears to be mediated by pLKB1 Ser428, and emerged as a possible mechanism contributing to the association between BRAF mutation and mTOR pathway up-regulation. When we evaluated the rapamycin in the growth of thyroid cancer cell lines, we detected that cell lines with activating mutations in the MAPK pathway show a higher sensitivity to this drug. Conclusions: We determined that the AKT/mTOR pathway is particularly overactivated in human cPTC harboring the BRAFV600E mutation. Moreover, our results suggest that the mTOR pathway could be a good target to enhance therapy effects in certain types of thyroid carcinoma, namely in those harboring the BRAFV600E mutation.

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