Growth suppression of esophageal cancer cells by p16INK4 and p15INK4B in vitro.
OBJECTIVE
We investigate whether p16INK4 and p15INK4B inhibit cellular proliferation and exert a growth suppressive effect on esophageal cancer cells.


METHODS
The growth suppressive effects of p16INK4 and p15INK4B were evaluated by transfecting vectors containing the p16INK4 cDNA or the p15INK4B cDNA, or both, constitutively driven by a cytomegalovirus promoter, into two human esophageal cancer cell lines containing or lacking endogenous p16INK4 and/or p15INK4B.


RESULTS
These experiments demonstrated that in both cells lines tested, the numbers of cells surviving dramatically decreased in p16INK4-transfected and p15INK4B-transfected cells compared with control vector-transfected cells. There was no significant difference in the degree of growth inhibition between p16INK4-transfected and pI5INK4B-transfected cell lines.


CONCLUSIONS
These results suggest that p16INK4 and p15INK4B play important roles in the initiation or promotion of esophageal cancer. The inactivation of p16INK4 and p15INK4B may contribute to uncontrolled growth in human cancer.
Zhou
X
X
Department of Medicine/GI Division, University of Maryland School of Medicine and Veterans Affairs Hospital, Baltimore, Maryland 21201, USA.
Suzuki
H
H
Lei
J
J
Cole
K
K
Yin
J
J
Suzuki
V
V
Abraham
J M
JM
Shimada
Y
Y
Imamura
M
M
Chan
T
T
Hannon
G J
GJ
Meltzer
S J
SJ
D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology*; D049109:Cell Proliferation; D050762:Cyclin-Dependent Kinase Inhibitor p15 / Q000235:genetics / Q000502:physiology*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics / Q000502:physiology*; D004938:Esophageal Neoplasms / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D066298:In Vitro Techniques; D014162:Transfection; D014407:Tumor Cells, Cultured
D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16