|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Th e role of ferroptosis in ionizing radiation-induced cell death and tumor suppression显示文摘Ferroptosis,a form of regulated cell death caused by lipid peroxidation,was recently identified as a natural tumor suppression mechanism.Here,we show that ionizing radiation(IR)induces ferroptosis in cancer cells.Mechanistically,IR induces not only reactive oxygen species(ROS)but also the expression of ACSL4,a lipid metabolism enzyme required for ferroptosis,resulting in elevated lipid peroxidation and ferroptosis.ACSL4 ablation largely abolishes IR-induced ferroptosis and promotes radioresistance.IR also induces the expression of ferroptosis inhibitors,including SLC7A11 and GPX4;as an adaptive response.IR-or KEAP1 deficiencyinduced SLC7A11 expression promotes radioresistance through inhibiting ferroptosis.Inactivating SLC7A11 or GPX4 with ferroptosis inducers(FINs)sensitizes radioresistant cancer cells and xenograft tumors to IR.Furthermore,radiotherapy induces ferroptosis in cancer patients,and increased ferroptosis correlates with better response and longer survival to radiotherapy in cancer patients.Our study reveals a previously unrecognized link between IR and ferroptosis and indicates that further exploration of the combination of radiotherapy and FINs in cancer treatment is warranted. | Guang Lei Yilei Zhang Pranavi Koppula Xiaoguang Liu Jie Zhang Steven HLin Jaffer AAjani Qin Xiao Zhongxing Liao Hui Wang Boyi Gan | 2020 | Cell Research2020，30，2： | 88 |
| 2 | Cystine transporter SLC7A11/xCT in cancer:ferroptosis,nutrient dependency,and cancer therapy显示文摘The cystine/glutamate antiporter SLC7A11(also commonly known as xCT)functions to import cystine for glutathione biosynthesis and antioxidant defense and is overexpressed in multiple human cancers.Recent studies revealed that SLC7A11 overexpression promotes tumor growth partly through suppressing ferroptosis,a form of regulated cell death induced by excessive lipid peroxidation.However,cancer cells with high expression of SLC7A11(SLC7A11^(high))also have to endure the significant cost associated with SLC7A11-mediated metabolic reprogramming,leading to glucose-and glutamine-dependency in SLC7A11^(high) cancer cells,which presents potential metabolic vulnerabilities for therapeutic targeting in SLC7A11^(high) cancer.In this review,we summarize diverse regulatory mechanisms of SLC7A11 in cancer,discuss ferroptosis-dependent and-independent functions of SLC7A11 in promoting tumor development,explore the mechanistic basis of SLC7A11-induced nutrient dependency in cancer cells,and conceptualize therapeutic strategies to target SLC7A11 in cancer treatment.This review will provide the foundation for further understanding SLC7A11 in ferroptosis,nutrient dependency,and tumor biology and for developing novel effective cancer therapies. | Pranavi Koppula Li Zhuang Boyi Gan | 2021 | Protein & Cell2021，12，8： | 97 |
| 3 | Amino acid transporter SLC7A11/ xCT at the crossroads of regulating redox homeostasis and nutrient dependency of cancer显示文摘Cancer cells often upregulate nutrient transporters to fulfill their increased biosynthetic and bioenergetic needs,and to maintain redox homeostasis.One nutrient transporter frequently overexpressed in human cancers is the cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xCT).SLC7A11 promotes cystine uptake and glutathione biosynthesis,resulting in protection from oxidative stress and ferroptotic cell death.Recent studies have unexpectedly revealed that SLC7A11 also plays critical roles in glutamine metabolism and regulates the glucose and glutamine dependency of cancer cells.This review discusses the roles of SLC7A11 in regulating the anti-oxidant response and nutrient dependency of cancer cells,explores our current understanding of SLC7A11 regulation in cancer metabolism,and highlights key open questions for future studies in this emerging research area.A deeper understanding of SLC7A11 in cancer metabolism may identify new therapeutic opportunities to target this important amino acid transporter for cancer treatment. | Pranavi Koppula Yilei Zhang Li Zhuang Boyi Gan | 2018 | Cancer Communications2018，38，1： | 77 |
| 4 | Ferroptosis,radiotherapy,and combination therapeutic strategies显示文摘Ferroptosis,an iron-dependent form of regulated cell death driven by peroxidative damages of polyunsatu-rated-fatty-acid-containing phospholipids in cellular membranes,has recently been revealed to play an important role in radiotherapy-induced cell death and tumor suppression,and to mediate the synergy between radiotherapy and immunotherapy.In this review,we summarize known as well as putative mechanisms underlying the crosstalk between radiotherapy and fer-roptosis,discuss the interactions between ferroptosis and other forms of regulated cell death induced by radiotherapy,and explore combination therapeutic strategies targeting ferroptosis in radiotherapy and immunotherapy.This review will provide important frameworks for future investigations of ferroptosis in cancer therapy. | Guang Lei Chao Mao Yuelong Yan Li Zhuang Boyi Gan | 2021 | Protein & Cell2021，12，11： | 29 |
| 5 | NADPH debt drives redox bankruptcy:SLC7A11/xCT-mediated cystine uptake as a double-edged sword in cellular redox regulation显示文摘Cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xCT)plays a key role in antioxidant defense by mediating cystine uptake,promoting glutathione synthesis,and maintaining cell survival under oxidative stress conditions.Recent studies showed that,to prevent toxic buildup of highly insoluble cystine inside cells,cancer cells with high expression of SLC7A11(SLC7A11high)are forced to quickly reduce cystine to more soluble cysteine,which requires substantial NADPH supply from the glucose-pentose phosphate pathway(PPP)route,thereby inducing glucose-and PPP-dependency in SLC7A11high cancer cells.Limiting glucose supply to SLC7A11high cancer cells results in significant NADPH“debt”,redox“bankruptcy”,and subsequent cell death.This review summarizes our current understanding of NADPH-generating and-consuming pathways,discusses the opposing role of SLC7A11 in protecting cells from oxidative stresseinduced cell death such as ferroptosis but promoting glucose starvationeinduced cell death,and proposes the concept that SLC7A11-mediated cystine uptake acts as a double-edged sword in cellular redox regulation.A detailed understanding of SLC7A11 in redox biology may identify metabolic vulnerabilities in SLC7A11high cancer for therapeutic targeting. | Xiaoguang Liu Yilei Zhang Li Zhuang Kellen Olszewski Boyi Gan | 2021 | Genes & Diseases2021，8，6： | 7 |
| 6 | Cytochrome P450 reductase(POR)as a ferroptosis fuel显示文摘Oxygen,iron,and polyunsaturated fatty acids(PUFAs;fatty acids containing more than one double bond)are all beneficial to our cellular lives.Incorporation of these components into cellular processes,however,comes at a cost:the bis-allylic structure of PUFAs and the enrichment of cellular environments with iron and oxygen render PUFA-containing phospholipids(PUFA-PLs)particularly susceptible to peroxidation(Yang and Stockwell,2016). | Pranavi Koppula Li Zhuang Boyi Gan | 2021 | Protein & Cell2021，12，9： | 2 |
| 7 | PKCβII-ACSL4 pathway mediating ferroptosis execution and anti-tumor immunity显示文摘Ferroptosis is an iron-dependent form of regulated cell death that results from oxidative damages of membrane phospholipids,and is mechanistically and morphologically unique compared to other cell death modalities,such as apoptosis and necroptosis[1].Excessive ferroptosis is indicative of many pathological conditions,including cardiovascular diseases,neurodegenerative diseases,and acute organ injury,whereas ferroptosis impairment has been shown to fuel tumor progression and metastasis;therefore,targeting ferroptosis represents a promising strategy for treating these diseases[2-10].Ferroptosis is triggered by a lethal accumulation of lipid peroxides on the cell membrane. | Guang Lei Amber Horbath Zhuang Li Boyi Gan | 2022 | Cancer Communications2022，42，7： | 2 |
| 8 | FAK-mediated src phosphorylation of endophilin A2 inhibits endocytosis of MT1-MMP and promotes ECM degradation 显示文摘 | Wu Xiaoyang Gan Boyi Yoo Youngdong | 2005 | Dev Cell2005，9，2： | 1 |
| 9 | 位于氧化还原稳态调控和癌症营养依赖性十字路口的氨基酸转运蛋白SLC7A11/xCT显示文摘癌细胞经常会上调营养转运蛋白的表达,以满足它们日益增加的生物合成和生物能量需求,并维持氧化还原的动态平衡。在人类癌症中有一种经常过表达的营养转运蛋白,是胱氨酸/谷氨酸逆向转运蛋白溶质载体家族7成员11(solute carrier family 7 member 11,SLC7A11,也称为xCT)。SLC7A11促进胱氨酸摄取和谷胱甘肽生物合成,从而防止氧化应激和细胞铁死亡。最近的研究意外地揭示了SLC7A11在谷氨酰胺代谢中也起着关键作用,并调节癌细胞的葡萄糖和谷氨酰胺依赖性。本文综述了SLC7A11在调节癌细胞抗氧化反应和营养依赖中的作用,探讨了SLC7A11在肿瘤代谢中的调控作用,并提出了这一新兴研究领域中有待进一步研究的关键问题。对癌症代谢中SLC7A11的更深入了解可能会为这种重要的氨基酸转运蛋白靶向癌症治疗提供新的治疗机会。 | Pranavi Koppula Yilei Zhang Li Zhuang Boyi Gan | 2018 | 癌症2018，37，10： | 1 |
| 10 | ACSL4,PUFA,and ferroptosis:new arsenal in anti-tumor immunity显示文摘In a recent study published in Cancer Cell,Liao et al.1 identified CD8+T-cell-derived interferon(IFN)γin combination with polyunsaturated fatty acids(PUFAs)as a natural ferroptosis inducer(FIN)to trigger tumor ferroptosis and promote anti-tumor immunity in an acyl-coenzyme A synthetase long-chain family member 4(ACSL4)-dependent manner.Ferroptosis refers to a form of regulated cell death triggered by excessive iron-dependent peroxidation of PUFA-containing phospholipids(PUFA-PLs)in the cellular membrane. | Boyi Gan | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 1 |
| 11 | How erastin assassinates cells by ferroptosis revealed显示文摘Ferroptosis represents an oxidative form of iron-dependent cell death resulting from unrestrained peroxidized phospholipids on cellular membranes(Jiang et al.,2021).In recent years,research interest in ferroptosis has increased steeply partly due to its high relevance to diverse diseases(such as cancer and neurodegener-ative diseases)and the enormous potential of ferroptosis induc-ers and inhibitors to treat these diseases(Jiang et al.,2021;Tang et al.,2021. | Boyi Gan | 2023 | Protein & Cell2023，14，2： | 0 |
| 12 | FSP1 oxidizes NADPH to suppress ferroptosis显示文摘Dear Editor,Ferroptosis is a form of non-apoptotic cell death characterized by the accumulation of iron-dependent lipid peroxides and oxidative damage to cell membrane.1 Discovered relative recently,ferroptosis is morphologically and mechanistically distinct from other forms of cell death,such as apoptosis,necroptosis,and pyroptosis.2 Ferroptosis has been implicated in various pathological conditions,including neurodegenerative diseases,cancer,and ischemia-reperfusion injury.3,4,5 Thus,studying ferroptosis could not only provide insights into the fundamental mechanisms of cell death and survival,but also identify new targets for therapeutic intervention in a variety of pathological conditions. | Sitao Zhang Shengsong Gou Qian Zhang Xin Yong Boyi Gan Da Jia | 2023 | Cell Research2023，33，12： | 0 |
| 13 | Phospholipase iPLA2β acts as a guardian against ferroptosis显示文摘Ferroptosis,a form of iron-dependent regulated cell death caused by excessive accumulation of lipid hydroperoxides,has been associated with various pathological conditions and diseases[1].Excessive ferroptosis has been causally associated with acute kidney injury,cardiovascular,neurodegenerative and hepatic diseases,whereas impaired ferroptosis in premalignant cells has been shown to contribute to tumor development[2,3].To escape from ferroptotic cell death,cells have been equipped with several antioxidant defense systems against lipid peroxidation(Figure 1).Glutathione peroxidase 4(GPX4)suppresses ferroptosis by converting lipid hydroperoxides into non-toxic lipid alcohols at the expense of its cofactor glutathione(GSH)[4].Ferroptosis suppressor protein-1(FSP1,also known as AIFM2),a NAD(P)H-dependent oxidoreductase located on the plasma membrane,catalyzes the reduction of ubiquinone to ubiquinol,a radical trapping antioxidant that suppresses ferroptosis independent of the GSH-GPX4 axis[5,6].In addition,dihydroorotate dehydrogenase(DHODH),an enzyme involved in the de novo pyrimidine biosynthesis pathway,inhibits ferroptosis by reducing ubiquinone to ubiquinol in the inner mitochondrial membrane[7]. | Chao Mao Guang Lei Li Zhuang Boyi Gan | 2021 | Cancer Communications2021，41，11： | 0 |
| 14 | Ferroptosis as an important driver of lupus显示文摘Systemic lupus erythematosus(SLE),the most common form of lupus,is a chronic autoimmune disorder characterized by a global loss of self-tolerance and hyper-activation of both innate and adaptive immune systems(Kaul et al.,2016).Neutrophils,the most abundant leukocytes in human blood,have a critical role in maintaining immune surveillance and tissue homeostasis,and its dysregulation is of high relevance to SLE(Ricklin et al.,2010).In patients with SLE,accelerated neutrophil death and the deficiency in clearing dying neutrophils cause nuclear and cytoplasmic antigen exposure,excessive production of type I interferon(IFN),and neutrophil extracellular trap(NET)release,subsequently inducing autoimmune responses(Garcia-Romo et al.,2011).Dysregulated neutrophil death is believed to be a major cause of SLE;however,the underlying mechanism of neutrophil death in SLE is not well-defined. | Chao Mao Guang Lei Li Zhuang Boyi Gan | 2022 | Protein & Cell2022，13，5： | 0 |
| 15 | Uncovering the IL-1β-PCAF-NNT axis:A new player in ferroptosis and tumor immune evasion显示文摘Chronic inflammation is recognized as a crucial hallmark of cancer.Interleukin-1β(IL-1β),one of the proinflammatory cytokines,plays an ambiguous or even contradictory role in cancer development[1].While increased expression of IL-1βin the tumor microenvironment is associated with tumor development,and invasiveness[1],it has also shown anti-tumorigenic effects in other contexts[2].Therefore,it is difficult to define IL-1β’s role as either tumor-promoting or anti-tumorigenic in cancers.Further investigation of IL-1βin specific contexts is essential to comprehensively understand its role in cancers. | Qidong Li Boyi Gan | 2023 | Cancer Communications2023，43，9： | 0 |
| 16 | Ether phospholipids govern ferroptosis显示文摘Ferroptosis is a cell death modality triggered by excessive lipid peroxidation.Two recent studies(Zou et al.,2020;Cui et al.,2021)not only reveal critical roles of ether-linked phospholipids as an additional source for providing polyunsaturated fatty acid-containing phospholipids in driving ferroptosis but also suggest a context-dependent role of TMEM189-mediated vinyl-ether phospholipid(plasmalogen)synthesis in ferroptosis. | Hyemin Lee Li Zhuang Boyi Gan | 2021 | Journal of Genetics and Genomics2021，48，7： | 0 |
| 17 | Hyperoxidized PRDX3 as a specific ferroptosis marker显示文摘The lack of a reliable and specific marker for ferroptosis has hindered the advancement of treatments related to this cell death mechanism toward clinical application.A recent study published in Molecular Cell has identified hyperoxidized perox-iredoxin 3(PRDX3)as a promising marker for ferroptosis,open-ing up new avenues for monitoring and targeting ferroptosis in disease treatment. | Yuelong Yan Boyi Gan | 2023 | Life Metabolism2023，2，6： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员