The molecular mechanism of cohosh extract from Kunming animals in inhibiting triple-negative breast cancer

  ERα/PR/HER2 triple-negative breast cancer (TNBC) is the worst type of breast cancer. At present, the treatment of TNBC is still at the level of traditional chemotherapy, and patients have a high recurrence rate after treatment and are easy to metastasize. There is an urgent need to find new therapeutic targets and effective drugs to improve the survival rate of TNBC patients. Apoptosis is the main way anti-cancer drugs kill cancer cells. Screening monomer components that induce apoptosis of TNBC cells from medicinal plants will lay the foundation for the development of new anti-cancer drugs. Cimicifuga L plants are widely distributed in Asia, Europe and North America, and are used as medicinal plants in different ethnic regions of our country. The underground rhizomes are used to clear away heat and detoxify, and treat sore throat, toothache and gynecology. Diseases etc. Cohosh can be used to treat syndromes such as menopausal syndrome and osteoporosis. The triterpenoids extracted from cohosh have anti-tumor, AIDS, malaria, blood lipid and other biological activities.

   The Kunming Institute of Zoology, Chinese Academy of Sciences, and the team of researcher Qiu Minghua from the Kunming Institute of Botany, Chinese Academy of Sciences, conducted a collaborative study to extract a large number of new triterpenoid monomer compounds from the rhizome of green cohosh, but they have not studied their tumor suppressor activity. The first authors of the study, Yanjie Kong and Fubing Li, screened a large number of compounds and found that KHF16 can effectively inhibit the survival of TNBC cell lines in vitro. Further research found that KHF16 can significantly induce cell proliferation of MDA-MB-468 and SW527, block the cell cycle of cancer cells in G2/M phase, and induce apoptosis at the same time. KHF16 can reduce the expression levels of XIAP, Mcl-1, Survivin and Cyclin B1/D1. Mechanism studies have found that KHF16 inhibits the NF-κB signaling pathway in TNBC cells. KHF16 strongly blocked the phosphorylation of IKKα/β and IKBα, the entry of p65 into the nucleus and the expression of NF-κB downstream target genes including XIAP, Mcl-1 and Survivin.