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321.
Faisal Thayyullathil Anees Rahman Cheratta Ameer Alakkal Karthikeyan Subburayan Siraj Pallichankandy Yusuf A. Hannun Sehamuddin Galadari 《Cell death & disease》2021,12(1)
Ferroptosis is a type of regulated cell death characterized by ROS accumulation and devastating lipid peroxidation (LPO). The role of acid sphingomyelinase (ASM), a key enzyme in sphingolipid metabolism, in the induction of apoptosis has been studied; however, to date its role in ferroptosis is unclear. In this study, we report that ASM plays a hitherto unanticipated role in promoting ferroptosis. Mechanistically, Erastin (Era) treatment results in the activation of ASM and generation of ceramide, which are required for the Era-induced reactive oxygen species (ROS) generation and LPO. Inhibition of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) or removal of intracellular ROS, significantly reduced Era-induced ASM activation, suggesting that NADPH oxidase-derived ROS regulated ASM-initiated redox signaling in a positive feedback manner. Moreover, ASM-mediated activation of autophagy plays a critical role in ferroptosis inducers (FINs)-induced glutathione peroxidase 4 (GPX4) degradation and ferroptosis activation. Genetic or pharmacological inhibition of ASM diminishes Era-induced features of autophagy, GPX4 degradation, LPO, and subsequent ferroptosis. Importantly, genetic activation of ASM increases ferroptosis in cancer cells induced by various FINs. Collectively, these findings reveal that ASM plays a novel role in ferroptosis that could be exploited to improve pathological conditions that link to ferroptosis.Subject terms: Lipid peroxides, Cancer models, Macroautophagy, Lipid signalling 相似文献
322.
323.
Varshasnata Mohanty Yashwanth Subbannayya Shankargouda Patil Vinuth N. Puttamallesh Mohd. Altaf Najar Keshava K. Datta Sneha M. Pinto Sameera Begum Neeta Mohanty Samapika Routray Riaz Abdulla Jay Gopal Ray David Sidransky Harsha Gowda T. S. Keshava Prasad Aditi Chatterjee 《Journal of cell communication and signaling》2021,15(3):447
324.
Wagdy M. Eldehna Mahmoud F. Abo-Ashour Tarfah Al-Warhi Sara T. Al-Rashood Amal Alharbi Rezk R. Ayyad Khayal Al-Khayal Maha Abdulla Hatem A. Abdel-Aziz Rehan Ahmad Radwan El-Haggar 《Journal of enzyme inhibition and medicinal chemistry》2021,36(1):319
Mitochondrial anti-apoptotic Bcl2 and BclxL proteins, are overexpressed in multiple tumour types, and has been involved in the progression and survival of malignant cells. Therefore, inhibition of such proteins has become a validated and attractive target for anticancer drug discovery. In this manner, the present studies developed a series of novel isatin–indole conjugates (7a-j and 9a-e) as potential anticancer Bcl2 and BclxL inhibitors. The progression of the two examined colorectal cancer cell lines was significantly inhibited by all of the prepared compounds with IC50 ranges132–611 nM compared to IC50 = 4.6 µM for 5FU, against HT-29 and IC50 ranges 37–468 nM compared to IC50 = 1.5 µM for 5FU, against SW-620. Thereafter, compounds 7c and 7g were selected for further investigations. Interestingly, both compounds exhibited selective cytotoxicity against both cell lines with high safety to normal fibroblast (HFF-1). In addition, both compounds 7c and 7g induced apoptosis and inhibited Bcl2 and BclxL expression in a dose-dependent manner. Collectively, the high potency and selective cytotoxicity suggested that conjugates 7c and 7g could be a starting point for further optimisation to develop novel pro-apoptotic and antitumor agents towards colon cancer. 相似文献