OBJECTIVE This study aims to explore the anticancer effect of fisetin for breast cancer in vivo and in vitro.METHODS Viability of cultured breast cancer cells including 4T1,Mcf-7 and MDA-MB-231 were determined using MTT assay and electric cell-substrate impedance sensing(ECIS).Cell migratory ability was evaluated by wound healing assay.Cell apoptosis was quantified using the AnnexinⅤ/propidium iodide(PI)detection kit and analyzed by flow cytometry.Subsequently,the potential anti-tumor and anti-metastatic mechanism was investigated by Western blotting.Inhibition of tumor growth and metastasis was evaluated by assessment of tumor weight,volume and analysis of bioluminescent signal after a homograft inoculation.Oral,intraperitoneal were respectively administered in different media.RESULTS we found that fisetin inhibited the proliferation and induced apoptosis of breast cel lines.Our study showed that fisetin inhibited migration of breast cancer cells.Importantly,our data demonstrated theanticancer activity of fisetin by oral administration.In addition,the PI3K/AKT/m TORstatus in breast cancer cells may contribute to fisetin anticancer activity.CONCLUSION Fisetin exerts anti-tumor growth and anti-metastatic effects in breast cancer cells,that is,at least partly,associated with decreased downregulation of PI3K/AKT/m TOR expression,The absolute bioavailability of intraperitoneal administration is relatively lower than that of intragastric administration,the anticancer effect of fisetin in vivo needs more study to address the solubility issue. OBJECTIVE This study aims to explore the anticancer effect of fisetin for breast cancer in vivo and in vitro. METHODS Viability of cultured breast cancer cells including 4T1, Mcf-7 and MDA-MB-231 were determined using MTT assay and electric cell-substrate impedance sensing (ECIS). Cell migratory ability was evaluated by wound healing assay. Cell apoptosis was quantified using the Annexin V / propidium iodide (PI) detection kit and analyzed by flow cytometry. Published, the potential anti-tumor and anti-metastatic mechanism was investigated by Western blotting. Inhibition of tumor growth and metastasis was evaluated by assessment of tumor weight, volume and analysis of bioluminescent signal after a homograft inoculation. Oral, intraperitoneal were respectively administered in different media. RESULTS we found that fisetin inhibited the proliferation and induced apoptosis of breast cel lines. Our study showed that fisetin inhibited migration of breast cancer cells. Implantantly, our data said th eanticancer activity of fisetin by oral administration. In addition, the PI3K / AKT / m TORstatus in breast cancer cells may contribute to fisetin anticancer activity. CONCLUSION Fisetin exerts anti-tumor growth and anti-metastatic effects in breast cancer cells, that is, at The less likely, associated with decreased downregulation of PI3K / AKT / m TOR expression, The absolute bioavailability of intraperitoneal administration is relatively lower than that of intragastric administration, the anticancer effect of fisetin in vivo needs more study to address the solubility issue.