Q Peng1, S Jin, S Lu. 1. Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100021.
Abstract
OBJECTIVE: To explore the effect of p16 gene on the growth inhibition of esophageal carcinoma cell line NEC. METHODS: The full length of wild-type p16 cDNA was transfected into the esophageal carcinoma cell line of human fetus induced by N-methyl-N-benzylnitrosamine (NMBzA). In these esophageal carcinoma cell, p16 gene was homozygously deleted. RESULTS: Expression of exogenous p16 gene in NEC cells was identified by dot blot and Western blot analyses. The growth rate of NEC transfected with p16 gene (NEC-p16) was markedly suppressed. Colony formation in soft agar was also decreased significantly. Cell cycle analysis by flow cytometry showed that the number of cells in G1-G0 phase of NEC-p16 cells was significantly increased while cells in S and G2 + M phase was decreased compared to that of the control NEC cells. CONCLUSION: Transduction of wild type p16 gene into p16 gene-depleted esophageal cancer cells can restore its suppressive effect on cell growth by arrest of cell cycle at G1 phase.
OBJECTIVE: To explore the effect of p16 gene on the growth inhibition of esophageal carcinoma cell line NEC. METHODS: The full length of wild-type p16 cDNA was transfected into the esophageal carcinoma cell line of human fetus induced by N-methyl-N-benzylnitrosamine (NMBzA). In these esophageal carcinoma cell, p16 gene was homozygously deleted. RESULTS: Expression of exogenous p16 gene in NEC cells was identified by dot blot and Western blot analyses. The growth rate of NEC transfected with p16 gene (NEC-p16) was markedly suppressed. Colony formation in soft agar was also decreased significantly. Cell cycle analysis by flow cytometry showed that the number of cells in G1-G0 phase of NEC-p16 cells was significantly increased while cells in S and G2 + M phase was decreased compared to that of the control NEC cells. CONCLUSION: Transduction of wild type p16 gene into p16 gene-depleted esophageal cancer cells can restore its suppressive effect on cell growth by arrest of cell cycle at G1 phase.