Gentian violet inhibits MDA-MB-231 human breast cancer cell proliferation, and reverses the stimulation of osteoclastogenesis and suppression of osteoblast activity induced by cancer cells.

Abstract:

:Gentian violet (GV) is a cationic triphenylmethane dye, with potent antifungal and antibacterial activity. We recently reported that in vitro GV suppresses the differentiation of bone resorbing osteoclasts while stimulating the differentiation and activity of bone forming osteoblasts. Breast cancer is highly metastatic to bone and drives bone turnover that further promotes cancer engraftment and expansion, the so-called vicious cycle. In humans, breast cancer metastases cause osteolytic lesions and skeletal damage that leads to bone fractures, an additional source of patient morbidity. The MDA-MB-231 human breast cancer cell line is a commonly used model of human breast cancer that when injected into mice metastasizes to bone causing osteolytic lesions by promoting osteoclastic bone resorption and/or suppressing osteoblastic bone formation. In the present study, we investigated the direct action of GV on MDA-MB-231 proliferation, and the capacity of GV to reverse the negative impact of MDA-MB-231 cells on osteoclast and osteoblast differentiation. Our data reveal for the first time that GV suppresses proliferation, and induces apoptosis, of MDA-MB-231 cells. We further demonstrated the capacity of GV to reverse the pro-osteoclastogenic and anti-osteoblastic activities of MDA-MB-231 cells in vitro. These data suggest that GV has important applications in the treatment of breast cancer through multiple actions including direct suppression of cancer cell proliferation, breaking the vicious cycle between cancer and bone, and alleviating the skeletal defects induced by bone metastasis.

journal_name

Oncol Rep

journal_title

Oncology reports

authors

Yamaguchi M,Vikulina T,Weitzmann MN

doi

10.3892/or.2015.4190

subject

Has Abstract

pub_date

2015-10-01 00:00:00

pages

2156-62

issue

4

eissn

1021-335X

issn

1791-2431

journal_volume

34

pub_type

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