Human telomerase is absent in most normal tissues, but is abnormally activated 
in all major cancer cells. Telomerase enables tumor cells to maintain telomere 
length, allowing indefinite replicative capacity. Albeit not sufficient in 
itself to induce neoplasia, telomerase is believed to be necessary for cancer 
cells to grow without limit. Studies using an antisense oligonucleotide (ASODN) 
to the RNA component of telomerase or human telomerase reverse transcriptase 
(hTERT) demonstrate that telomerase in human tumor lines can be blocked in vivo. 
Inhibition of hTERT led to telomere shortening and cancer cell death, validating 
telomerase as a target for anticancer genetic therapy. Varieties of approaches 
for hTERT inhibition have been investigated. The aim of this study was to 
analyze the biological activity of ASODN to the hTERT mediated by retrovirus 
vector, which was used as therapy for ovarian tumor. We constructed and 
characterized a recombinant retrovirus vector with full-length hTERT antisense 
complementary DNA. The vector was introduced into ES-2 by lipofectamine-mediated 
gene transfection. The cellular proliferation and telomerase activity of the 
transformant cells were retarded. The hTERT gene expression and the telomerase 
activity of the transformant cells were both decreased. The transformant cells 
show partial reversion of the malignant phenotype. PT67 cells were also 
transfected with the recombinant vector and virus-producer cells were generated. 
The retrovirus-containing supernatant effectively inhibited the growth of human 
ovarian tumor xenografts in mouse models (subcutaneous tumor model), and 
enhanced the mouse survival time.