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2017 ; 11
(7
): 878-891
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The EMT spectrum and therapeutic opportunities
#MMPMID28544151
Voon DC
; Huang RY
; Jackson RA
; Thiery JP
Mol Oncol
2017[Jul]; 11
(7
): 878-891
PMID28544151
show ga
Carcinomas are phenotypically arrayed along an epithelial-mesenchymal transition
(EMT) spectrum, a developmental program currently exploited to understand the
acquisition of drug resistance through a re-routing of growth factor signaling.
This review collates the current approaches employed in developing therapeutics
against cancer-associated EMT, and provides an assessment of their respective
strengths and drawbacks. We reflect on the close relationship between EMT and
chemoresistance against current targeted therapeutics, with a special focus on
the epigenetic mechanisms that link these processes. This prompts the hypothesis
that carcinoma-associated EMT shares a common epigenetic pathway to cellular
plasticity as somatic cell reprogramming during tissue repair and regeneration.
Indeed, their striking resemblance suggests that EMT in carcinoma is a
pathological adaptation of an intrinsic program of cellular plasticity that is
crucial to tissue homeostasis. We thus propose a revised approach that targets
the epigenetic mechanisms underlying pathogenic EMT to arrest cellular plasticity
regardless of upstream cancer-driving mutations.
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