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2016 ; 7
(45
): 74015-74030
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium
entry in lung adenocarcinoma
#MMPMID27677589
Qi L
; Song W
; Li L
; Cao L
; Yu Y
; Song C
; Wang Y
; Zhang F
; Li Y
; Zhang B
; Cao W
Oncotarget
2016[Nov]; 7
(45
): 74015-74030
PMID27677589
show ga
Several fibroblast growth factor (FGF) isoforms act to stimulate
epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7
are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC)
cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell
morphology, promoted EMT-associated protein expression, and enhanced cell
proliferation, migration/invasion and colony initiation. In addition, FGF4
increased store-operated calcium entry (SOCE) and expression of the calcium
signal-associated protein Orai1. The SOCE inhibitor 2,5-di-tert-butylhydroquinone
(BHQ) or Orai1 knockdown reversed all of the EMT-promoting effects of FGF4. BHQ
also inhibited FGF4-induced EMT in a mouse xenograft model. Finally, 60 human
lung ADC samples and 21 sets of matched specimens (primary and metastatic foci in
lymph nodes from one patient) were used to confirm the clinicopathologic
significance of FGF4 and its correlation with E-cadherin, Vimentin and Orai1
expression. Our study thus shows that FGF4 induces EMT by elevating SOCE in lung
ADC.