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Role of phospho-ezrin in differentiating thyroid carcinoma.

ABSTRACT: Comprehensive theory explaining the relationship between estrogen (E2) and ezrin in metastasis of thyroid cancer remains non-elicited. In vitro results revealed that E2 could stimulate the expression and phosphorylation of ezrin in a time and dose dependent manner. Our data clearly showed that E2 enhanced the migration and invasion of cells, which was reversed by the transfection of cells with ezrin specific siRNA. Further, we observed that Phosphoinositide 3-kinase (PI3K) ROCK-2 are among the kinases responsible for E2 induced phosphorylation of ezrin. Clinical validation of ezrin/phospho-ezrin revealed that phospho-ezrin was intensely expressed in follicular thyroid carcinoma (FTC) and follicular variant of papillary thyroid carcinoma (FVPTC), while it was completely absent in follicular adenoma (FA) lesions in which the differentiation of the follicular neoplasms remains subtle. When histology of different carcinomas is correlated with benign FA with respect to phospho-ezrin, we observed that the marker was highly significant (p?=?0.0001). 100% sensitivity, specificity and diagnostic accuracy of the above marker in the histological association of FTC, FVPTC with FA, enables us to suggest phospho-ezrin as a diagnostic marker to differentiate the follicular neoplasms. These data are the first to suggest the dynamic regulation of ezrin phosphorylation during metastasis in FTC.

SUBMITTER: Lathika LM

PROVIDER: S-EPMC6470213 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Role of phospho-ezrin in differentiating thyroid carcinoma.

Lathika Lakshmi Mohan LM Nair Jagathnath Krishna Kumarapillai Mohanan JKKM Saritha Valliamma Neelakandapilla VN Sujathan Kunjuraman K Sreeja Sreeharshan S

Scientific reports 20190417 1

Comprehensive theory explaining the relationship between estrogen (E2) and ezrin in metastasis of thyroid cancer remains non-elicited. In vitro results revealed that E2 could stimulate the expression and phosphorylation of ezrin in a time and dose dependent manner. Our data clearly showed that E2 enhanced the migration and invasion of cells, which was reversed by the transfection of cells with ezrin specific siRNA. Further, we observed that Phosphoinositide 3-kinase (PI3K) ROCK-2 are among the k ...[more]

PMID: 30996241

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Project description:BackgroundThe cyclin-dependent-kinase inhibitors (CDKN)/retinoblastoma (RB1) pathway has been implicated as having a role in medullary thyroid carcinoma (MTC) tumorigenesis. CDKN2C loss has been associated with RET-mediated MTC in humans but with minimal phenotypic correlation provided. The objective of this study was to evaluate the association between tumor RET mutation status, CDKN2C loss, and aggressiveness of MTC in a cohort of patients with sporadic disease.MethodsTumors from patients with sporadic MTC treated at a single institution were evaluated for somatic RETM918T mutation and CDKN2C copy number loss. These variables were compared to patient demographics, pathology detail, clinical course, and disease-specific and overall survival.ResultsSixty-two MTC cases with an initial surgery date ranging from 1983 to 2009 met the inclusion criteria, of whom 36 (58%) were male. The median age at initial surgery was 53 years (range 22-81 years). The median tumor size was 30 mm (range 6-145 mm) with 29 (57%) possessing extrathyroidal extension. Nodal and/or distant metastasis at presentation was found in 47/60 (78%) and 12/61 (20%) patients, respectively. Median follow-up time was 10.5 years (range 1.1-27.8 years) for the censored observations. The presence of CDKN2C loss was associated with worse M stage and overall AJCC stage. Median overall survival of patients with versus without CDKN2C loss was 4.14 [confidence interval (CI) 1.93-NA] versus 18.27 [CI 17.24-NA] years (p < 0.0001). Median overall survival of patients with a combined somatic RETM918T mutation and CDKN2C loss versus no somatic RETM918T mutation and CDKN2C loss versus somatic RETM918T mutation and CDKN2C 2N versus no somatic RETM918T mutation and CDKN2C 2N was 2.38 [CI 1.67-NA] years versus 10.81 [CI 2.46-NA] versus 17.24 [CI 9.82-NA] versus not reached [CI 13.46-NA] years (p < 0.0001).ConclusionsThe detection of somatic CDKN2C loss is associated with the presence of distant metastasis at presentation as well decreased overall survival, a relationship enhanced by concomitant RETM918T mutation. Further defining the genes involved in the progression of metastatic MTC will be an important step toward identifying pathways of disease progression and new therapeutic targets.

Dataset Information

Role of phospho-ezrin in differentiating thyroid carcinoma.

Publications

Role of phospho-ezrin in differentiating thyroid carcinoma.

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