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2017 ; 14
(3
): 3117-3123
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Glutaminase sustains cell survival via the regulation of glycolysis and
glutaminolysis in colorectal cancer
#MMPMID28928849
Song Z
; Wei B
; Lu C
; Li P
; Chen L
Oncol Lett
2017[Sep]; 14
(3
): 3117-3123
PMID28928849
show ga
Cancer cells remodel their metabolic programs towards aerobic glycolysis and
elevated glutaminolysis to meet the requirement s of rapid proliferation.
Understanding how cells sense and adapt to these changes may provide new targets
for therapeutic intervention. Deamination of glutamine to glutamate by
glutaminase (GLS1) is an essential step in glutaminolysis. The present study
revealed that the loss of GLS1 expression by RNA interference or inhibitor
decreased the proliferation and viability of colorectal cancer (CRC) cells. The
abrogation of GLS1 function notably inhibited glutaminolysis and aerobic
glycolysis, which resulted in the decrease of internal ATP levels and an increase
in cell death. In addition, GLS1 expression was significantly elevated in CRC
tissues in comparison with adjacent normal tissues (P<0.001), which is associated
with the cell differentiation status and tumor node metastasis stage. In
conclusion, the present study defined a key role of GLS1 in coupling
glutaminolysis with elevated glucose uptake and consequently the growth of colon
cancer cells. Due to the functional importance of GLS1 in regulating cell
metabolism, it was proposed that GLS1 may serve as a target for colorectal cancer
therapy.