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2016 ; 7
(15
): 19631-42
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Ezrin contributes to cervical cancer progression through induction of
epithelial-mesenchymal transition
#MMPMID26933912
Kong J
; Di C
; Piao J
; Sun J
; Han L
; Chen L
; Yan G
; Lin Z
Oncotarget
2016[Apr]; 7
(15
): 19631-42
PMID26933912
show ga
Cervical cancer is the third most common cancer in females worldwide. The
treatment options for advanced cervical cancer are limited, leading to high
mortality. Ezrin is a membrane-cytoskeleton-binding protein recently reported to
act as a tumor promoter, and we previously indicated that the aberrant
localization and overexpression of Ezrin could be an independent effective
biomarker for prognostic evaluation of cervical cancers. In this study, we
identified Ezrin as a regulator of epithelial-mesenchymal transition (EMT) and
metastasis in cervical cancer. Ezrin knock-down inhibited anchorage-independent
growth, cell migration, and invasion of cervical cancer cell lines in vitro and
in vivo. EMT was inhibited in Ezrin-depleted cells, with up-regulation of
E-cadherin and Cytokeratin-18 (CK-18) and down-regulation of mesenchymal markers.
Ezrin knock-down also induced Akt phosphorylation. These results implicate Ezrin
as an EMT regulator and tumor promoter in cervical cancer, and down-regulation of
Ezrin suppressed cervical cancer progression, possibly via the phosphoinositide
3-kinase/Akt pathway. Furthermore, the expression pattern of Ezrin protein was
closely related with the lymphovascular invasion status of cervical cancer by
immunohistochemistry, and the survival analysis revealed that the cervical cancer
patients with the perinuclear Ezrin expression pattern had longer survival time
than those with the cytoplasmic Ezrin expression pattern. Ezrin thus represents a
promising target for the development of novel and effective strategies aimed at
preventing the progression of cervical cancer.
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