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2017 ; 49
(1
): 87-96
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Inactivation of Capicua drives cancer metastasis
#MMPMID27869830
Okimoto RA
; Breitenbuecher F
; Olivas VR
; Wu W
; Gini B
; Hofree M
; Asthana S
; Hrustanovic G
; Flanagan J
; Tulpule A
; Blakely CM
; Haringsma HJ
; Simmons AD
; Gowen K
; Suh J
; Miller VA
; Ali S
; Schuler M
; Bivona TG
Nat Genet
2017[Jan]; 49
(1
): 87-96
PMID27869830
show ga
Metastasis is the leading cause of death in people with lung cancer, yet the
molecular effectors underlying tumor dissemination remain poorly defined. Through
the development of an in vivo spontaneous lung cancer metastasis model, we show
that the developmentally regulated transcriptional repressor Capicua (CIC)
suppresses invasion and metastasis. Inactivation of CIC relieves repression of
its effector ETV4, driving ETV4-mediated upregulation of MMP24, which is
necessary and sufficient for metastasis. Loss of CIC, or an increase in levels of
its effectors ETV4 and MMP24, is a biomarker of tumor progression and worse
outcomes in people with lung and/or gastric cancer. Our findings reveal CIC as a
conserved metastasis suppressor, highlighting new anti-metastatic strategies that
could potentially improve patient outcomes.
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