Objective     To explore the molecular mechanism of inhibited malignant phenotype by knock-down of apurinic/apyrimidinic endonuclease (APE1) in human osteosarcoma cell HOS

as well as the possible interacting molecules among APE1.      Methods     Knock-down of APE1 by synthesized APE1 siRNA in HOS cell was identified first by Western blotting and AP endonuclease assay

then the gene profile was determined with GEArray

TM

series Human CancerPathwayFinder gene array.      Results     The specific knock-down of APE1 was found in HOS cell transfected with APE1 siRNA

and its inhibited rate was 91.5%. Six biological pathways of the

gene array were involved in HOS cell after knock-down of APE1

but the cell cycle pathway was less influenced. Forty-two out of 96 genes were altered (43.8%)

in which only CDK4

FGFR2

KAI1 and NCAM were increased

38 others were decreased.      Conclusion     The knock-down of APE1 was detected to be involved in all the pathways including cell cycle and DNA repair

apoptosis

signal transduction

adhesion

angiogenesis

invasion and metastasis. These findings are significant to further elucidate APE1 role in tumor genesis and to provide experimental evidence for gene therapy targeting APE1 gene in the future.