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2017 ; 108
(6
): 1240-1252
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Chloride intracellular channel 1 regulates the antineoplastic effects of
metformin in gallbladder cancer cells
#MMPMID28378944
Liu Y
; Wang Z
; Li M
; Ye Y
; Xu Y
; Zhang Y
; Yuan R
; Jin Y
; Hao Y
; Jiang L
; Hu Y
; Chen S
; Liu F
; Zhang Y
; Wu W
; Liu Y
Cancer Sci
2017[Jun]; 108
(6
): 1240-1252
PMID28378944
show ga
Metformin is the most commonly used drug for type 2 diabetes and has potential
benefit in treating and preventing cancer. Previous studies indicated that
membrane proteins can affect the antineoplastic effects of metformin and may be
crucial in the field of cancer research. However, the antineoplastic effects of
metformin and its mechanism in gallbladder cancer (GBC) remain largely unknown.
In this study, the effects of metformin on GBC cell proliferation and viability
were evaluated using the Cell Counting Kit-8 (CCK-8) assay and an apoptosis
assay. Western blotting was performed to investigate related signaling pathways.
Of note, inhibition, knockdown and upregulation of the membrane protein Chloride
intracellular channel 1 (CLIC1) can affect GBC resistance in the presence of
metformin. Our data demonstrated that metformin apparently inhibits the
proliferation and viability of GBC cells. Metformin promoted cell apoptosis and
increased the number of early apoptotic cells. We found that metformin can exert
growth-suppressive effects on these cell lines via inhibition of p-Akt activity
and the Bcl-2 family. Notably, either dysfunction or downregulation of CLIC1 can
partially decrease the antineoplastic effects of metformin while upregulation of
CLIC1 can increase drug sensitivity. Our findings provide experimental evidence
for using metformin as an antitumor treatment for gallbladder carcinoma.
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