Phosphatase and tensin homolog deleted on chromosome 10 inhibits cholangiocarcinoma cell QBC939 proliferation through regulating amplified in breast cancer 1 and phosphatidylinositol 3 kinase/protein kinase B signaling pathway

Abstract

Objective To investigate the effects of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) on proliferation of cholangiocarcinoma cell QBC939 and the mechanisms by which PTEN regulates QBC939 cell proliferation. Methods QBC939 cells were transfected with 4 μg PTEN vector or small interfering RNA (siRNA) for 72 h. Then methyl thiazol tetrazolium (MTT) assays was used to detect the ability of cells proliferation and Western blotting was performed to detect the protein levels of amplified in breast cancer 1 (AIB1) and significant molecular marker of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) signal pathway after PTEN was overexperssed or downregulated by siRNA in QBC939 cells. Results After 72 h transfection, the absorbance (A) value of PTEN-overexpressed group (0.216±0.013) was lower than that of the control group (0.243±0.002, P=0.026), which indicated that the proliferation of QBC939 cells was inhibited, meanwhile the expression of AIB1 and phosphorylated Akt (p-Akt) which was phosphorylated in PI3K/Akt signal pathway was significantly decreased. Down-regulation of PTEN through siRNA resulted in that its A value (0.403±0.011) was lower than that of the control group (0.490±0.033, P=0.013), which promoted the proliferation of QBC939 cells, and that up-regulated the expression of AIB1 and p-Akt. Conclusion These results suggest that PTEN inhibited cholangiocarcinoma cell proliferation through regulating AIB1 and PI3K/Akt signaling pathway. Key words: Cholangiocarcinoma; Tensin homolog deleted on chromosome 10; Amplified in breast cancer 1; Phosphatidylinositol 3 kinase/protein kinase B; Proliferation