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TCF7L2 positively regulates aerobic glycolysis via the EGLN2/HIF-1? axis and
indicates prognosis in pancreatic cancer
#MMPMID29476053
Xiang J
; Hu Q
; Qin Y
; Ji S
; Xu W
; Liu W
; Shi S
; Liang C
; Liu J
; Meng Q
; Liang D
; Ni Q
; Xu J
; Zhang B
; Yu X
Cell Death Dis
2018[Feb]; 9
(3
): 321
PMID29476053
show ga
Patients with pancreatic ductal adenocarcinoma have much worse prognoses, and
much effort has been directed toward understanding the molecular biological
aspects of this disease. Accumulated evidence suggests that constitutive
activation of the Wnt/?-catenin signalling contributes to the oncogenesis and
progression of pancreatic cancer. Transcription factor 7-like2/transcription
factor 4 (TCF7L2/TCF4), a ?-catenin transcriptional partner, plays a vital role
in the Wnt/?-catenin signalling pathway. In the present study, we investigated
the clinicopathological significance of TCF7L2 in pancreatic cancer. Our results
demonstrated that patients with higher TCF7L2 expression had worse prognosis. Our
in vitro studies demonstrated that TCF7L2 positively regulated aerobic glycolysis
by suppressing Egl-9 family hypoxia inducible factor 2 (EGLN2), leading to
upregulation of hypoxia inducible factor 1 alpha subunit (HIF-1?). The impact of
TCF7L2 on aerobic glycolysis was further confirmed in vivo by assessing (18)FDG
uptake in pancreatic cancer patients and in a subcutaneous xenograft mouse model.
In summary, we identified novel predictive markers for prognosis and suggest a
previously unrecognized role for TCF7L2 in control of aerobic glycolysis in
pancreatic cancer.
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