Yuebawei refers to 8 kinds of genuine medicinal materials in south China area，namely Citri Grandis Exocarpium， Citrus reticulata， Amomum villosum， Pogostemon cablin， Morinda officinalis， Aquilaria sinensis， Citrus medica and Polygonum multiflorum. The results of this review show that， the pharmacological effects of Yuebawei are very extensive. It has significant effects in relieving cough and phlegm， anti-bacterial and anti-inflammatory， enhancing immunity， anti-oxidation， antidepressant， immune regulation and regulating gastrointestinal function. Its development and application prospects are broad， but most of the existing pharmacological studies stay on pharmacodynamic studies. In the aspect of the safety research of Yuebawei， there are few studies on the safety of other medicinal materials， except for the liver toxicity of P. multiflorum； at the same time， there are few comparative studies on the therapeutic advantages of Yuebawei and other local medicinal materials in clinical application. It is necessary to strengthen the research on the material basis of pharmacological action mechanism， and safety and efficacy observation of clinical medication for Yuebawei， so as to provide scientific basis for the development of new drugs and clinical promotion and application of Yuebawei.

As the most aggressive breast cancer, triple-negative breast cancer (TNBC) is still incurable and very prone to metastasis. The transform growth factor β (TGF-β)-induced epithelial-mesenchymal transition (EMT) is crucially involved in the growth and metastasis of TNBC. This study reported that a natural compound isotoosendanin (ITSN) reduced TNBC metastasis by inhibiting TGF-β-induced EMT and the formation of invadopodia. ITSN can directly interact with TGF-β receptor type-1 (TGFβR1) and abrogated the kinase activity of TGFβR1, thereby blocking the TGF-β-initiated downstream signaling pathway. Moreover, the ITSN-provided inhibition on metastasis obviously disappeared in TGFβR1-overexpressed TNBC cells in vitro as well as in mice bearing TNBC cells overexpressed TGFβR1. Furthermore, Lys232 and Asp351 residues in the kinase domain of TGFβR1 were found to be crucial for the interaction of ITSN with TGFβR1. Additionally, ITSN also improved the inhibitory efficacy of programmed cell death 1 ligand 1 (PD-L1) antibody for TNBC in vivo via inhibiting the TGF-β-mediated EMT in the tumor microenvironment. Our findings not only highlight the key role of TGFβR1 in TNBC metastasis, but also provide a leading compound targeting TGFβR1 for the treatment of TNBC metastasis. Moreover, this study also points out a potential strategy for TNBC treatment by using the combined application of anti-PD-L1 with a TGFβR1 inhibitor.