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Additive growth inhibitory effects of ibandronate and antiestrogens in estrogen receptor-positive breast cancer cell lines.

Abstract：

INTRODUCTION:Bisphosphonates are inhibitors of osteoclast-mediated tumor-stimulated osteolysis, and they have become standard therapy for the management of bone metastases from breast cancer. These drugs can also directly induce growth inhibition and apoptosis of osteotropic cancer cells, including estrogen receptor-positive (ER+) breast cancer cells. METHODS:We examined the anti-proliferative properties of ibandronate on two ER+ breast cancer cell lines (MCF-7 and IBEP-2), and on one ER negative (ER-) cell line (MDA-MB-231). Experiments were performed in steroid-free medium to assess ER regulation and the effect of ibandronate in combination with estrogen or antiestrogens. RESULTS:Ibandronate inhibited cancer cell growth in a dose- and time-dependent manner (approximate IC50: 10(-4) M for MCF-7 and IBEP-2 cells; 3 x 10(-4) M for MDA-MB-231 cells), partly through apoptosis induction. It completely abolished the mitogenic effect induced by 17beta-estradiol in ER+ breast cancer cells, but affected neither ER regulation nor estrogen-induced progesterone receptor expression, as documented in MCF-7 cells. Moreover, ibandronate enhanced the growth inhibitory action of partial (4-hydroxytamoxifen) and pure (ICI 182,780, now called fluvestrant or Faslodex) antiestrogens in estrogen-sensitive breast cancer cells. Combination analysis identified additive interactions between ibandronate and ER antagonists. CONCLUSION:These data constitute the first in vitro evidence for additive effects between ibandronate and antiestrogens, supporting their combined use for the treatment of bone metastases from breast cancer.

journal_name

Breast Cancer Res

journal_title

Breast cancer research : BCR

authors

Journe F,Chaboteaux C,Magne N,Duvillier H,Laurent G,Body JJ

doi

10.1186/bcr1363

keywords:

subject

Has Abstract

pub_date

2006-01-01 00:00:00

pages

R2

issue

1

eissn

1465-5411

issn

1465-542X

pii

bcr1363

journal_volume

8

pub_type

杂志文章

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