Grant-in-Aid for Scientific Research (C)
In the present study, anti bone metastasis agents which have different targets, was examined to identify the mechanisms for the induction of CSCs in the bone MI. Treatment of bone modifying agents, targeting osteoclasts, did not change the ratio of CSCs in the bone ME as well as subQ ME and treatment of TGFβ signaling inhibitor, significantly reduced that of CSC in the bone ME. Interestingly, inappropriate treatments of anti cancer agent or androgen, targeting prostate cancer cells, significantly increased the ratio of CSCs in the bone ME in our model using androgen independent or dependent prostate cancer cells. Our results indicated that bone MI would be good niche for CSCs, and TGFβ would be involved in the induction of CSCs, and anti-cancer agents combined with those targeting CSC may plays a key role to eliminate the drug resistant bone metastasis of prostate or breast cancer.
Int'l Joint Research
Proceedings of the National Academy of Sciences of the United States of America
International Journal of Molecular Sciences
Pathol Int. 2017 Nov;67(11):564-574.
Advanced Drug Delivery Reviews, Epub
Volume: 99, Part B,
J. Interferon & Cytokine Res
Attribution of KAKENHI