Autophagy activation in breast cancer cells in vitro after the treatment with PI3K/AKT/mTOR inhibitors

Introduction . Current chemotherapy of breast cancer has a wide range disadvantages, in particular, the development therapy-related infections and hormonal imbalance. Combination main cytostatic with glucocorticoids allows to broaden its therapeutic interval decrease total toxicity treatment. However, long-term treatment leads severe side effects via activation multiple molecular mechanisms. Thus, activate prosurvival mTOR-dependent autophagy. Therefore, evaluation PI3K (phosphoinositide 3-kinases) / Akt (protein kinase B) mTOR (mammalian target rapamycin) inhibitors as adjuvants for therapy is important optimization protocol. Aim Analysis PI3K/Akt/mTOR inhibitors, rapamycin, wortmannin LY-294002 combination cell lines different subtypes. Materials methods We demonstrated inhibition signaling autophagy induction after cells by Western blotting analysis Beclin-1, phospho-Beclin-1 (Ser93 Ser30). Conclusion Dexamethasone cooperatively inhibited activated vitro.