Cancer stem cells in either an in vitro or in vivo
Cancer stem cells in either an in vitro or in vivo model [31]. Because FAK is known to interact with the Src family members and its activation is reported to be suppressed by dasatinib, the inhibitory effect of dasatinib on the FAK signaling pathway might explain the anti-stem cell activity of dasatinib. Further studies are clearly needed to elucidate the mechanism of action of dasatinib responsible for its anti-stem cell activity.Conclusions To the best of our knowledge, the present study has offered clear evidence that the Src inhibitor dasatinib preferentially inhibited the growth of breast cancer cells of the basal B subtype associated with a G1-S cell cycle blockade and a reduction in the proportion of ALDH1positive, putative breast cancer stem cells. In addition, dasatinib significantly enhanced an anti-tumor activity of one of DNA-damaging agents Eto in breast cancer cells of the basal B subtype. These strong PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28667899 preclinical findings warrant clinical trials using dasatinib and Eto in patients with breast cancer of the basal B subtype.Additional materialAdditional file 1: Table 1. Biological characteristics of breast cancer cell lines Additional file 2: Table 2. The 50 growth inhibitory concentrations of dasatinib or chemotherapeutic agents in breast cancer cell lines Additional file 3: Table 3. Proportion of breast cancer stem cells measured by immunocytochemistry and Aldefluor assay Additional file 4: Supplementary Figure 1. Additive antitumor activity of dasatinib and SN38 in MDA-MB-231 cells. Additional file 5: Supplementary Figure 2. Additive antitumor activity of dasatinib and SN38 in MDA-MB-157 cells. Additional file 6: Supplementary Figure 3. Additive antitumor activity of dasatinib and Pac in MDA-MB-231 cells. Additional file 7: Supplementary Figure 4. Additive antitumor activity of dasatinib and Pac in MDA-MB-157 cells.Acknowledgements This work was supported by Research GW856553X web Project Grants (20-112H and 21-103) from Kawasaki Medical School, by a Grant from the Japanese Breast Cancer Society and by a Grant from the Ministry of Education, Culture, Sports, Science, and Technology, Japan (20591561). The authors thank Mrs. Kimiko Hagihara and Ms. Megumi Ogo for their technical assistance. Author details 1 Department of Breast and Thyroid Surgery, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan. 2Department of Pathology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan. 3Department of Pathology, Tohoku University Hospital, 1-1 Seiryomachi, Aoba-ku, Sendai 980-8574, Japan. Authors’ contributions JK, NK, TM, YK, and MW made substantial contributions to the conception and design of the study, acquisition of data, and analysis and interpretation of the data. JK, NK, TM, and HS were involved in drafting the manuscript or revising it. All authors read and approved the final manuscript.Kurebayashi et al. BMC Cancer 2010, 10:568 http://www.biomedcentral.com/1471-2407/10/Page 10 ofCompeting interests The authors declare that they have no competing interests. Received: 4 February 2010 Accepted: 20 October 2010 Published: 20 October 2010 References 1. Perou CM, S lie T, Eisen MB, van de Rijn M, Jeffrey SS, Rees CA, Pollack JR, Ross DT, Johnsen H, Akslen LA, Fluge O, Pergamenschikov A, Williams C, Zhu SX, L ning PE, B resen-Dale AL, Brown PO, Botstein D: Molecular portraits of human breast tumours. Nature 2000, 406:747-52. 2. S lie T, Perou CM, Tibshirani R, Aas T, Geisler S, Johnsen H, Hasti.
