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PMID: 10766196 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

1,25-Dihydroxyvitamin D3 and all-trans-retinoic acid sensitize breast cancer cells to chemotherapy-induced cell death.

Cancer research ·Vol. 60 ·No. 7 ·2000-04-01 ·Pages 2040-8

Wang Q, Yang W, Uytingco MS, Christakos S, Wieder R

Abstract

We investigated the capacity of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and all-trans-retinoic acid (ATRA) to sensitize three breast cancer cell lines to the cell killing effects of paclitaxel (Taxol) and Adriamycin, two chemotherapeutic agents commonly used in the treatment of breast cancer. In tissue culture colony assays, 1,25(OH)2D3 and ATRA were synergistic in inhibiting the clonogenicity of MCF-7 and T-47D cells that expressed estrogen receptor; vitamin D receptor; retinoic acid receptors (RARs) alpha, beta, and gamma; and retinoid X receptors alpha, beta, and gamma but were not additive in MDA-MB-231 cells that lacked expression of estrogen receptor, RARalpha, and RARbeta. The hormones used individually or in combination induced up to 40-50% cell death by a trypan blue exclusion assay in a dose-dependent manner up to concentrations of 10(-7) M in MCF-7 and T-47D cells, more modestly in MDA-MB-231 cells, and not at all in MCF-10 and MCF-12 nontransformed mammary epithelial cells. Pretreating the cancer cell lines with 1,25(OH)2D3 and ATRA individually or in combination for 3 days prior to a 1-h incubation with paclitaxel or Adriamycin decreased the ED50 for inhibition of colony formation or for cell death by trypan blue by up to 2 logs for paclitaxel and up to 1 log for Adriamycin in all three cell lines but had no effect on chemotherapy-induced MCF-12 cell death. The effects of the hormones were synergistic with those of the chemotherapy agents in all of the breast cancer cell lines, generally at the higher concentrations. Cell death took place by apoptosis. To determine one potential reason for the greater potentiation of the effects of paclitaxel than those of Adriamycin, we determined the effects of preincubation of MCF-7 cells on paclitaxel-induced phosphorylation of Bcl-2. Pretreatment of MCF-7 cells with either 1,25(OH)2D3 or ATRA increased the phosphorylation of Bcl-2 by variable concentrations of paclitaxel. These data suggest that pretreatment of breast cancer with 1,25(OH)2D3 or ATRA lowers the threshold for cell killing by chemotherapy agents and may provide a novel treatment option for this disease.

MeSH Terms
Antineoplastic Agents/toxicity Breast Neoplasms Calcitriol/toxicity Cell Survival/drug effects Doxorubicin/toxicity Drug Synergism Female Humans Paclitaxel/toxicity Receptors, Calcitriol/physiology Receptors, Estrogen/physiology Receptors, Retinoic Acid/physiology Retinoid X Receptors Transcription Factors/physiology Tretinoin/toxicity Tumor Cells, Cultured
Chemicals
Antineoplastic Agents Receptors, Calcitriol Receptors, Estrogen Receptors, Retinoic Acid Retinoid X Receptors Transcription Factors Tretinoin Doxorubicin Calcitriol Paclitaxel
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Wang Q
Department of Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103, USA.
Yang W
Uytingco M S
Christakos S
Wieder R
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
2000-04-01
Pages
2040-8
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
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