Induction of apoptosis and inhibition of telomerase activity in human bone marrow and HL-60 p53 null cells treated with anti-cancer drugs

Results showed that after exposure to the drugs, HL-60 cells as well as the human progenitors underwent a block in G2 and subsequently apoptosis, whereas stromal cells from bone marrow did not undergo a block in G2 or enter apoptosis after etoposide exposure. Telomere length increased in stromal cells after treatment with both etoposide and taxol whereas in HL-60 cells only after etoposide treatment with. Bax, bcl-2 and bcl-x change their expression in stromal cells, whereas bcl-x was induced after drug treatment and bcl-2 down regulated in progenitor cells. Our data suggest that telomerase activity and apoptosis are correlated and they seem to be modulated by a common gene, bcl-2.