摘要：Purpose: The study investigates the therapeutic effect of Oridonin on PTEN loss and HER2 amplification PI3K/AKT signaling hyper-activated (p-AKTHigh) breast cancer. Methods: The experiment uses MDAMB231, MCF-10A, SKBR3 (HER2 amplification), MDAMB468 (PTEN loss) cells, and Xenograft Murine Models. Cell viability is assessed by MTT, Clonogenic growth, CCK-8 assays. The inhibition of phosphorylation is tested by Western blot. Xenograft studies are used to test tumor growth blockage.The most possible result: Oridonin inhibits phosphorylation of AKT1 substrates and downstream proteins instead of AKT1. Also, it blocks the growth of PTEN loss and HER2 amplification p-AKTHigh breast cancer. Conclusion: This study provides important information for the clinical trial of Oridonin. Future experiments should focus on its toxicity and efficacy.
