Published in:
01-04-2015 | Research Article
1-butyltryptophan inhibits cell proliferation, migration, and
invasion through the Akt pathway in human gastric cancer cells
Authors:
Ting Sun, Hua Tian, YangXun Xin
Published in:
Tumor Biology
|
Issue 4/2015
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Abstract
We have previously demonstrated that novel 1-alkyl-tryptophan analogs
1-butyltryptophan (1-BT) can serve as a potential antitumor agent. However, the
molecular mechanisms of 1-BT on cancer cells remain to be elucidated. The effect of
1-BT on cell proliferation was detected by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl
tetrazolium bromide (MTT) assay and clone formation assay in SGC7901 and AGS cells.
Cell cycle was determined by flow cytometry. Cell migration and invasion was
determined by wound healing assay and transwell assay. The expression of
cyclin-dependent kinase 4 (CDK4), cyclin D1, p16, PCNA, phosphorylated Akt, total
Akt, phosphorylated ERK1/2, and total ERK1/2 was examined using Western blotting.
Our data demonstrated that 1-BT inhibited cell proliferation in a dose- and
time-dependent manner by the downregulation of expression of cyclin D1 and CDK4 and
by the upregulation of p16 expression. The inhibition of cell growth was also
demonstrated by cell cycle arrest at the G1/S phase. Furthermore, 1-BT inhibited
cell migration and invasion in SGC7901 cells. In addition, we found that
phosphorylated Akt was suppressed in 1-BT treated SGC7901 cells. Overexpression of
activated Akt reversed the effects of 1-BT on cell migration and invasion in SGC7901
cells. These results indicated that 1-BT inhibited gastric cancer cells
proliferation and migration through the Akt pathway, which has the potential
clinical significance in the prevention and treatment of gastric cancer.