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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Transl+Res
2016 ; 8
(4
): 1641-58
Nephropedia Template TP
gab.com Text
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English Wikipedia
Galectin-1 mediates TGF-?-induced transformation from normal fibroblasts into
carcinoma-associated fibroblasts and promotes tumor progression in gastric
cancer
#MMPMID27186290
Zheng L
; Xu C
; Guan Z
; Su X
; Xu Z
; Cao J
; Teng L
Am J Transl Res
2016[]; 8
(4
): 1641-58
PMID27186290
show ga
Rcinoma-associated fibroblasts (CAFs) are a major constituent of the tumor
microenvironment. Cancer cells can induce the transformation from normal
fibroblasts (NFs) into CAFs, reciprocally, CAFs promote tumor invasion and
proliferation. TGF-? has been the mostly accepted factor to fuel NFs
transformation into CAFs. Galectin-1 (Gal1) is highly upregulated in CAFs of
multiple human cancers, and overexpression of Gal1 in CAFs promotes tumor
progression. The effect of Gal1 on TGF-?-induced CAFs activation has not yet been
established in gastric cancer (GC). In this study, we show that Gal1 expression
in stroma is positively related to TGF-? in epithelial cells by retrospective
analysis of GC patient samples. Meanwhile, conditioned media (CMs) from gastric
cancer cells induce expression of both Gal1 and the CAFs marker alpha smooth
muscle actin (?-SMA) in NFs via TGF-? secretion. Knockdown of Gal1 prevents
TGF-?-induced the conversion of NFs to CAFs. CMs from fibroblasts overexpressing
Gal1 inhibits cancer cells apoptosis, promotes migration and invasion in vitro.
Thus, Gal1 is significantly involved in the development of tumor-promoting
microenvironment by enhancing TGF-? signaling in a positive feedback loop.
Targeting Gal1 in tumor stroma should be considered as a potential therapeutic
target for GC.