Enhanced cytotoxic activity of doxorubicin through the inhibition of autophagy in triple negative breast cancer cell line

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• 作者：Seyma Aydinlik ; MSc^a ; Merve Erkisa ; MSc^a ; Buse Cevatemre ; MSc^a ; Mehmet Sarimahmut ; PhD^a ; Egemen Dere ; PhD^a ; Ferda Ari ; PhD^a ; Engin Ulukaya ; MD^b ; ^{eulukaya@istinye.edu.tr}
• 关键词：TNBC ; triple negative breast cancer ; ROS ; reactive oxygen species ; H2DCFDA ; 2&prime ; 7&prime ; -dichlorodihydrofluorescein diacetate ; MTT ; 3-[4 ; 5-dimethyl-2-thiazolyl]-2 ; 5-diphenyl-2H-tetrazolium bromide ; CI value ; combination index value ; DXR ; doxorubicin ; 3-MA ; 3-methyladenine ; PI3K ; phosphoinositide 3-kinase ; PI ; propidium iodide ; Nec-1 ; necrostatin ; MLKL ; mixed lineage kinase domain-like ; RIPK1 ; receptor-TNFRSF-interacting serine threonine kinase1 ; TNFRSF10A ; Tumor necrosis factor receptor sup
• 刊名：Biochimica et Biophysica Acta (BBA) - General Subjects
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：1861
• 期：2
• 页码：49-57
• 全文大小：1107 K
• 卷排序：1861

文摘

DXR induces autophagy as a survival mechanism in MDA-MB-231 cells. Suppression of the cytoprotective form of autophagy by 3-MA, enhances the cytotoxic activity of DXR in MDA-MB-231 cells. Combination of 3-MA and DXR seems to result in RIP1-mediated necroptotic cell death, while DXR alone induces apoptosis. The SAPK/JNK kinase activation and increased ROS levels play an important role during necroptosis in MDA-MB-231 cells. Combination of 3-MA and DXR is proposed for the management of triple negative breast cancer due to its synergistic growth-inhibitory effect in vitro.