Oridonin, an AKT1 Inhibitor, Suppresses the Growth of Breast Cancers with Hyperactivation of PI3K/AKT Signaling

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. Ce...

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Bibliographic Details
Main Authors: Liu, Xin-Yu, Zhang, Lizi
Format: Conference Proceeding
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
AKT1 protein
Amplification
Animal models
Breast cancer
Cell culture
Cell viability
Cholecystokinin
Downstream effects
ErbB-2 protein
Phosphorylation
PTEN protein
Signaling
Substrate inhibition
Toxicity
Xenografts
Xenotransplantation
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Summary: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.
ISSN:2267-1242
2555-0403
2267-1242
DOI:10.1051/e3sconf/202127103014