Upregulation of BNIP3 promotes apoptosis of lung cancer cells that were induced by p53.
It has been shown that p53 induces cell apoptosis and the Bcl-2 family plays key roles in this process. However, the molecular mechanism of p53 apoptotic pathway is still unclear. Here, we show that overexpression of exogenous wild-type p53 induced apoptosis in lung cancer cells and high metastasis potential cells had a faster rate of apoptosis than low metastasis potential cells. The expression of pro-apoptotic gene BNIP3 was increased significantly both in Anip973 and 95D cell lines which have high metastasis ability, but not AGZY83-a or little increased in 95C cell lines which possess low metastasis ability. Overexpression of BNIP3 increases apoptotic rate induced by p53 in AGZY83-a cells. Blocking the expression of BNIP3 by siRNA in Anip973 cells decreased apoptotic rate mediated by p53. Taken together, these data suggest that high level expression of BNIP3 mediated rapid apoptosis that was triggered by p53 in lung cancer cells.
Yan
Jin
J
Laboratory of Medical Genetics, Harbin Medical University, China
Yun
Huang
H
Yang
Yu
Y
Jing
Bai
B
Feng
Chen
C
Song-bin
Fu
F
D017209:Apoptosis; D045744:Cell Line, Tumor; D019254:Genes, bcl-2; D016158:Genes, p53; D006801:Humans; D008175:Lung Neoplasms; D008565:Membrane Proteins / Q000096:biosynthesis*; D009362:Neoplasm Metastasis; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis*; D015854:Up-Regulation
C090121:BNIP3 protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins