Scientific Reports 2019 Apr 17;9(1):6190. | https://doi.org/10.1038/s41598-019-42612-0
Lakshmi Mohan Lathika, Jagathnath Krishna Kumarapillai Mohanan Nair, Valliamma Neelakandapilla Saritha, Kunjuraman Sujathan & Sreeharshan Sreeja
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.