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2015 ; 10
(3
): 1343-1349
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Metformin inhibits growth of lung adenocarcinoma cells by inducing apoptosis via
the mitochondria-mediated pathway
#MMPMID26622674
Wang J
; Gao Q
; Wang D
; Wang Z
; Hu C
Oncol Lett
2015[Sep]; 10
(3
): 1343-1349
PMID26622674
show ga
Metformin is commonly used to treat type II diabetes, although it may also reduce
the risk of cancer and improve the associated prognosis. However, its mode of
action in cancer remains unclear. The present study evaluated the effects of
metformin on lung adenocarcinoma A549 cells and identified molecular mechanisms
of metformin activity. The A549 cells were treated with metformin at different
concentrations and cell viability was assayed by using an MTT assay. The cell
cycle and the apoptosis rate were assayed by flow cytometry. Nude mice were
transplanted with A549 cells and the tumor growth inhibition rate was detected.
Once the A549 cells had been treated with 20 mM metformin for 48 h, the cell
cycle was arrested in the G(0)/G(l) phase and the apoptosis rate was 20.57±3.16%.
The expression of the B-cell lymphoma (Bcl)-2 and Bcl-extra large proteins was
downregulated following metformin treatment, while Bax protein expression was
signi?cantly increased. Tumor size in the high-dose metformin and cisplatin plus
metformin groups was significantly smaller, and the inhibition rates were 41.3
and 72.9%, respectively, compared with the control group. These results indicated
that metformin displays anticancer activity against lung adenocarcinoma by
causing G(1) arrest of the cell cycle and subsequent cell apoptosis through the
mitochondria-dependent pathway in A549 cells. Furthermore, it was found that
metformin dramatically inhibited lung adenocarcinoma tumor growth in vivo. These
data suggest that metformin may become a potential cytotoxic drug in the
prevention and treatment of lung adenocarcinoma.
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