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2017 ; 3
(ä): 17069
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Epithelial-to-mesenchymal transition in gallbladder cancer: from clinical
evidence to cellular regulatory networks
#MMPMID29188076
Xu S
; Zhan M
; Wang J
Cell Death Discov
2017[]; 3
(ä): 17069
PMID29188076
show ga
Gallbladder cancer (GBC), with late diagnosis, rapid disease progression and
early metastasis, is a highly aggressive malignant tumor found worldwide.
Patients with GBC have poor survival, low curative resection rates and early
recurrence. For such a lethal tumor, uncovering the mechanisms and exploring new
strategies to prevent tumor progression and metastasis are critically important.
Epithelial-to-mesenchymal transition (EMT) has a prominent role in the early
steps of tumor progression and metastasis by initiating polarized epithelial cell
transition into motile mesenchymal cells. Accumulating evidence suggests that EMT
can be modulated by the cooperation of multiple mechanisms affecting common
targets. Signaling pathways, transcriptional and post-transcriptional regulation
and epigenetic alterations are involved in the stepwise EMT regulatory network in
GBC. Loss of epithelial markers, acquisition of mesenchymal markers and
dysregulation of EMT-inducing transcription factors (EMT-TFs) have been observed
and are associated with the clinicopathology and prognosis of GBC patients.
Therefore, EMT may be a detectable and predictable event for predicting GBC
progression and metastasis in the clinic. In this review, we will provide an
overview of EMT from the clinical evidence to cellular regulatory networks that
have been studied thus far in clinical and basic GBC studies.