Long-term exposure of HL60 cells to 1,25-dihydroxyvitamin D3 reduces their tumorigenicity: A model for cancer chemoprevention

Xuening Wang, Nicholas M. Ponzio, George P. Studzinski

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Several lines of evidence suggest that 1.25-dihydroxyvitamin D3 (1,25D3) may be important in chemoprevention of human cancer. Here, we show that human promyelocytic leukemia cells HL60 cultured in the presence of 30 nM 1,25D3 (30A cells) for 3 years exhibited a reduced rate of tumor growth when injected into nu/nu mice, while cells grown in 40 nM 1,25D3 (40AF cells) tailed to form detectable tumors in 11 out of the 12 inoculated mice. Interestingly, both 30A and 40AF cells grew approximately twice as fast as the parental HL60-G cells under tissue culture conditions, even in the presence of 1,25D3, to which they developed resistance. Testa of the susceptibility of these cells to natural killer (NK) cell cytotoxicity showed that 40AF, but not HL60-G or 30A cells, were targets for the murine spleen NK cells. However, lysis of 30A cells was also detected when human NK cells were used in this assay, though the effector-to-target cell ratio necessary to obtain significant lysis above background levels was higher for 30A (80:1) than for 40AF (10:1) cells. These results suggest a mechanism for the reported chemopreventive effects of sunlight-generated 1,25D3 or dietary vitamin D3.

Original languageEnglish (US)
Pages (from-to)399-404
Number of pages6
JournalProceedings of the Society for Experimental Biology and Medicine
Issue number4
StatePublished - Sep 1 1997

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

Fingerprint Dive into the research topics of 'Long-term exposure of HL60 cells to 1,25-dihydroxyvitamin D<sub>3</sub> reduces their tumorigenicity: A model for cancer chemoprevention'. Together they form a unique fingerprint.

Cite this