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Editorial Expression of Concern: The NAD+ salvage pathway modulates cancer cell viability via p73 社论表达关注:NAD+ 挽救途径通过 p73 调节癌细胞的活力。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.1038/s41418-024-01382-7
T. Sharif, D.-G. Ahn, R.-Z. Liu, E. Pringle, E. Martell, C. Dai, A. Nunokawa, M. Kwak, D. Clements, J. P. Murphy, C. Dean, P. Marcato, C. McCormick, R. Godbout, S. A. Gujar, P. W. K. Lee
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引用次数: 0
Myeloid Mir34a suppresses colitis-associated colon cancer: characterization of mediators by single-cell RNA sequencing 髓系 Mir34a 可抑制结肠炎相关性结肠癌:通过单细胞 RNA 测序确定介质的特征
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.1038/s41418-024-01380-9
Janine König, Matjaz Rokavec, Meryem Gülfem Öner-Ziegler, Ye Fei, Heiko Hermeking

We have previously shown that general deletion of the gene encoding the p53-inducible Mir34a microRNA enhances the number and invasion of colitis-associated colorectal cancers (CACs) in mice. Since the p53-pathway has been implicated in tumor-suppression mediated by cells in the tumor microenvironment (TME) we deleted Mir34a in myeloid cells and characterized CACs in these with scRNA-Seq (single cell RNA sequencing). This revealed an increase in specific macrophage subtypes, such as Cdk8+ macrophages and Mrc1+, M2-like macrophages. The latter displayed elevated expression of 21 known Mir34a target mRNAs, including Csf1r, Axl, Foxp1, Ccr1, Nampt, and Tgfbr2, and 32 predicted Mir34a target mRNAs. Furthermore, Mir34a-deficient BMDMs showed enhanced migration, elevated expression of Csf1r and a shift towards M2-like polarization when compared to Mir34a-proficient BMDMs. Concomitant deletion of Csf1r or treatment with a Csf1r inhibitor reduced the CAC burden and invasion in these mice. Notably, loss of myeloid Mir34a function resulted in a prominent, inflammatory CAC cell subtype, which displayed epithelial and macrophage markers. These cells displayed high levels of the EMT transcription factor Zeb2 and may therefore enhance the invasiveness of CACs. Taken together, our results provide in vivo evidence for a tumor suppressive role of myeloid Mir34a in CACs which is, at least in part, mediated by maintaining macrophages in an M1-like state via repression of Mir34a targets, such as Csf1r. Collectively, these findings may serve to identify new therapeutic targets and approaches for treatment of CAC.

我们之前已经证明,在小鼠体内全面删除编码 p53 诱导的 Mir34a microRNA 的基因会增加结肠炎相关性结直肠癌(CAC)的数量和侵袭性。由于 p53 通路与肿瘤微环境(TME)中的细胞介导的肿瘤抑制作用有关,我们删除了骨髓细胞中的 Mir34a,并用 scRNA-Seq(单细胞 RNA 测序)鉴定了这些细胞中的 CACs。结果显示,特定巨噬细胞亚型增多,如 Cdk8+ 巨噬细胞和 Mrc1+、M2 样巨噬细胞。后者显示出 21 种已知 Mir34a 靶 mRNA(包括 Csf1r、Axl、Foxp1、Ccr1、Nampt 和 Tgfbr2)和 32 种预测 Mir34a 靶 mRNA 的表达升高。此外,与 Mir34a 基因缺陷的 BMDMs 相比,Mir34a 基因缺陷的 BMDMs 表现出更强的迁移能力、更高的 Csf1r 表达以及向 M2 样极化的转变。同时删除 Csf1r 或使用 Csf1r 抑制剂可减少这些小鼠的 CAC 负担和侵袭。值得注意的是,髓系 Mir34a 功能的丧失导致了一种突出的炎性 CAC 细胞亚型,它显示了上皮细胞和巨噬细胞标记。这些细胞显示出高水平的 EMT 转录因子 Zeb2,因此可能会增强 CAC 的侵袭性。综上所述,我们的研究结果为髓系 Mir34a 在 CACs 中的肿瘤抑制作用提供了体内证据,这种作用至少部分是通过抑制 Mir34a 靶点(如 Csf1r)使巨噬细胞维持在 M1 样状态而介导的。总之,这些发现可能有助于确定治疗 CAC 的新靶点和方法。
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引用次数: 0
Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer 探索果糖代谢作为胰腺癌潜在治疗方法的可能性
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-15 DOI: 10.1038/s41418-024-01394-3
Chengqiang Wang, Lu Wang, Qing Zhao, Jiao Ma, Yitao Li, Junliang Kuang, Xintong Yang, Huichang Bi, Aiping Lu, Kenneth C. P. Cheung, Gerry Melino, Wei Jia

Excessive fructose intake has been associated with the development and progression of pancreatic cancer. This study aimed to elucidate the relationship between fructose utilization and pancreatic cancer progression. Our findings revealed that pancreatic cancer cells have a high capacity to utilize fructose and are capable of converting glucose to fructose via the AKR1B1-mediated polyol pathway, in addition to uptake via the fructose transporter GLUT5. Fructose metabolism exacerbates pancreatic cancer proliferation by enhancing glycolysis and accelerating the production of key metabolites that regulate angiogenesis. However, pharmacological blockade of fructose metabolism has been shown to slow pancreatic cancer progression and synergistically enhance anti-tumor capabilities when combined with anti-angiogenic agents. Overall, targeting fructose metabolism may prove to be a promising therapeutic approach in the treatment of pancreatic cancer.

果糖摄入过多与胰腺癌的发生和发展有关。本研究旨在阐明果糖利用与胰腺癌进展之间的关系。我们的研究结果表明,胰腺癌细胞利用果糖的能力很强,除了通过果糖转运体 GLUT5 吸收外,还能通过 AKR1B1 介导的多元醇途径将葡萄糖转化为果糖。果糖代谢通过加强糖酵解和加速产生调节血管生成的关键代谢物,加剧了胰腺癌的增殖。然而,药理作用阻断果糖代谢已被证明可减缓胰腺癌的进展,与抗血管生成药物联合使用可协同增强抗肿瘤能力。总之,以果糖代谢为靶点可能被证明是治疗胰腺癌的一种前景广阔的治疗方法。
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引用次数: 0
AKR1B1-dependent fructose metabolism enhances malignancy of cancer cells 依赖 AKR1B1 的果糖代谢会增强癌细胞的恶性程度
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-15 DOI: 10.1038/s41418-024-01393-4
Qing Zhao, Bing Han, Lu Wang, Jia Wu, Siliang Wang, Zhenxing Ren, Shouli Wang, Haining Yang, Michele Carbone, Changsheng Dong, Gerry Melino, Wen-Lian Chen, Wei Jia

Fructose metabolism has emerged as a significant contributor to cancer cell proliferation, yet the underlying mechanisms and sources of fructose for cancer cells remain incompletely understood. In this study, we demonstrate that cancer cells can convert glucose into fructose through a process called the AKR1B1-mediated polyol pathway. Inhibiting the endogenous production of fructose through AKR1B1 deletion dramatically suppressed glycolysis, resulting in reduced cancer cell migration, inhibited growth, and the induction of apoptosis and cell cycle arrest. Conversely, the acceleration of endogenous fructose through AKR1B1 overexpression has been shown to significantly enhance cancer cell proliferation and migration with increased S cell cycle progression. Our findings highlight the crucial role of endogenous fructose in cancer cell malignancy and support the need for further investigation into AKR1B1 as a potential cancer therapeutic target.

果糖代谢已成为导致癌细胞增殖的一个重要因素,然而,人们对癌细胞获得果糖的基本机制和来源仍然知之甚少。在这项研究中,我们证明癌细胞可以通过一种名为 AKR1B1 介导的多元醇途径将葡萄糖转化为果糖。通过 AKR1B1 基因缺失抑制内源性果糖的产生,可显著抑制糖酵解,从而减少癌细胞迁移、抑制生长、诱导细胞凋亡和细胞周期停滞。相反,通过 AKR1B1 的过表达加速内源性果糖的生成,则会显著增强癌细胞的增殖和迁移,并增加 S 细胞周期的进展。我们的研究结果突显了内源性果糖在癌细胞恶变中的关键作用,并支持将 AKR1B1 作为潜在癌症治疗靶点进行进一步研究的必要性。
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引用次数: 0
SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice SOX4 通过 EBF2 介导的小鼠产热基因程序促进棕色脂肪的发育和维持
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-15 DOI: 10.1038/s41418-024-01397-0
Shuai Wang, Ting He, Ya Luo, Kexin Ren, Huanming Shen, Lingfeng Hou, Yixin Wei, Tong Fu, Wenlong Xie, Peng Wang, Jie Hu, Yu Zhu, Zhengrong Huang, Qiyuan Li, Weihua Li, Huiling Guo, Boan Li

Brown adipose tissue (BAT) is critical for non-shivering thermogenesis making it a promising therapeutic strategy to combat obesity and metabolic disease. However, the regulatory mechanisms underlying brown fat formation remain incompletely understood. Here, we found SOX4 is required for BAT development and thermogenic program. Depletion of SOX4 in BAT progenitors (Sox4-MKO) or brown adipocytes (Sox4-BKO) resulted in whitened BAT and hypothermia upon acute cold exposure. The reduced thermogenic capacity of Sox4-MKO mice increases their susceptibility to diet-induced obesity. Conversely, overexpression of SOX4 in BAT enhances thermogenesis counteracting diet-induced obesity. Mechanistically, SOX4 activates the transcription of EBF2, which determines brown fat fate. Moreover, phosphorylation of SOX4 at S235 by PKA facilitates its nuclear translocation and EBF2 transcription. Further, SOX4 cooperates with EBF2 to activate transcriptional programs governing thermogenic gene expression. These results demonstrate that SOX4 serves as an upstream regulator of EBF2, providing valuable insights into BAT development and thermogenic function maintenance.

棕色脂肪组织(BAT)对非颤抖性产热至关重要,因此是一种治疗肥胖症和代谢性疾病的有效方法。然而,棕色脂肪形成的调控机制仍不完全清楚。在这里,我们发现 SOX4 是棕色脂肪团发育和产热程序所必需的。在BAT祖细胞(Sox4-MKO)或棕色脂肪细胞(Sox4-BKO)中缺失SOX4会导致BAT变白和急性冷暴露时体温过低。Sox4-MKO 小鼠生热能力的降低增加了它们对饮食引起的肥胖的易感性。相反,SOX4在BAT中的过表达会增强生热能力,从而抵消饮食引起的肥胖。从机理上讲,SOX4 激活了 EBF2 的转录,而 EBF2 决定了棕色脂肪的命运。此外,SOX4 在 S235 处被 PKA 磷酸化可促进其核转位和 EBF2 的转录。此外,SOX4 与 EBF2 相互配合,激活了热源基因表达的转录程序。这些结果表明,SOX4 是 EBF2 的上游调节因子,为 BAT 的发育和生热功能的维持提供了宝贵的见解。
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引用次数: 0
Inhibition of BAK-mediated apoptosis by the BH3-only protein BNIP5 纯 BH3 蛋白 BNIP5 抑制 BAK 介导的细胞凋亡
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-15 DOI: 10.1038/s41418-024-01386-3
Sebastian Rühl, Zhenrui Li, Shagun Srivastava, Luigi Mari, Clifford S. Guy, Mao Yang, Tudor Moldoveanu, Douglas R. Green

BCL-2 family proteins regulate apoptosis by initiating mitochondrial outer membrane permeabilization (MOMP). Activation of the MOMP effectors BAX and BAK is controlled by the interplay of anti-apoptotic BCL-2 proteins (e.g., MCL-1) and pro-apoptotic BH3-only proteins (e.g., BIM). Using a genome-wide CRISPR-dCas9 transactivation screen we identified BNIP5 as an inhibitor of BAK-, but not BAX-induced apoptosis. BNIP5 blocked BAK activation in different cell types and in response to various cytotoxic therapies. The BH3 domain of BNIP5 was both necessary and sufficient to block BAK activation. Mechanistically, the BH3 domain of BNIP5 acts as a selective BAK activator, but a poor de-repressor of complexes between BAK and pro-survival BCL-2 family proteins. By promoting the binding of activated BAK to MCL-1 or BCL-xL, BNIP5 inhibits apoptosis when BAX is absent. Based on our observations, BNIP5 can act functionally as an anti-apoptotic BH3-only protein.

BCL-2 家族蛋白通过启动线粒体外膜通透性(MOMP)来调节细胞凋亡。MOMP效应因子BAX和BAK的激活受抗凋亡BCL-2蛋白(如MCL-1)和促凋亡BH3蛋白(如BIM)的相互作用控制。通过全基因组 CRISPR-dCas9 转录激活筛选,我们发现 BNIP5 是 BAK(而非 BAX)诱导细胞凋亡的抑制剂。BNIP5 在不同类型的细胞中以及对各种细胞毒性疗法的反应中都能阻止 BAK 的活化。BNIP5的BH3结构域对阻断BAK的活化既是必要的,也是充分的。从机理上讲,BNIP5的BH3结构域是一种选择性的BAK激活剂,但对BAK与促生存的BCL-2家族蛋白之间的复合物的抑制作用较弱。通过促进活化的 BAK 与 MCL-1 或 BCL-xL 结合,当 BAX 缺失时,BNIP5 可抑制细胞凋亡。根据我们的观察,BNIP5 在功能上可作为一种抗凋亡的纯 BH3 蛋白。
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引用次数: 0
127aa encoded by circSpdyA promotes FA synthesis and NK cell repression in breast cancers 由 circSpdyA 编码的 127aa 可促进乳腺癌中的 FA 合成和 NK 细胞抑制作用
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-14 DOI: 10.1038/s41418-024-01396-1
Xinya Gao, Zicheng Sun, Xin Liu, Jiayue Luo, Xiaoli Liang, Huijin Wang, Junyi Zhou, Ciqiu Yang, Tiantian Wang, Jie Li

Lipid metabolism reprogram plays key roles in breast cancer tumorigenesis and immune escape. The underlying mechanism and potential regulator were barely investigated. We thus established an in vivo tumorigenesis model, mice-bearing breast cancer cells were treated with an ordinary diet and high-fat diet, species were collected and subjected to circRNA sequence to scan the potential circRNAs regulating the lipid metabolism. CircSpdyA was one of the most upregulated circRNAs and had the potential to encode a 127-aa micro peptide (referred to as 127aa). 127 aa promotes tumorigenesis through promoting the fatty acid de novo synthesis by directly binding to FASN. Single-cell sequence indicated 127aa inhibited NK cell infiltration and function. This was achieved by inhibiting the transcription of NK cell activators epigenetically. Moreover, lipid-laden from 127aa positive cancer cells transferred to NK cells inhibited the cytotoxicity. Taken together, circSpdyA encoded 127aa promotes fatty acid de novo synthesis through directly binding with FASN and induced NK cell repression by inhibiting the transcription of NK cell activators.

脂质代谢重编程在乳腺癌肿瘤发生和免疫逃逸中起着关键作用。但对其潜在机制和调控因子的研究却很少。因此,我们建立了一个体内肿瘤发生模型,用普通饮食和高脂饮食处理小鼠乳腺癌细胞,收集样本并进行circRNA序列分析,以扫描调控脂质代谢的潜在circRNA。CircSpdyA是上调最多的circRNA之一,有可能编码127 aa的微肽(简称127aa)。127 aa 通过直接与 FASN 结合促进脂肪酸从头合成,从而促进肿瘤发生。单细胞序列表明,127aa 能抑制 NK 细胞的浸润和功能。这是通过表观遗传抑制 NK 细胞激活剂的转录实现的。此外,127aa 阳性癌细胞中的脂质负载转移到 NK 细胞中也抑制了细胞毒性。综上所述,circSpdyA编码的127aa通过直接与FASN结合促进脂肪酸的从头合成,并通过抑制NK细胞激活因子的转录诱导NK细胞抑制。
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引用次数: 0
SLAMF7 (CD319) on activated CD8+ T cells transduces environmental cues to initiate cytotoxic effector cell responses 活化的 CD8+ T 细胞上的 SLAMF7 (CD319) 通过环境线索启动细胞毒性效应细胞反应
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-10 DOI: 10.1038/s41418-024-01399-y
Holger Lingel, Laura Fischer, Sven Remstedt, Benno Kuropka, Lars Philipsen, Irina Han, Jan-Erik Sander, Christian Freund, Aditya Arra, Monika C. Brunner-Weinzierl

CD8+ T-cell responses are meticulously orchestrated processes regulated by intercellular receptor:ligand interactions. These interactions critically control the dynamics of CD8+ T-cell populations that is crucial to overcome threats such as viral infections or cancer. Yet, the mechanisms governing these dynamics remain incompletely elucidated. Here, we identified a hitherto unknown T-cell referred function of the self-ligating surface receptor SLAMF7 (CD319) on CD8+ T cells during initiation of cytotoxic T-cell responses. According to its cytotoxicity related expression on T effector cells, we found that CD8+ T cells could utilize SLAMF7 to transduce environmental cues into cellular interactions and information exchange. Indeed, SLAMF7 facilitated a dose-dependent formation of stable homotypic contacts that ultimately resulted in stable cell-contacts, quorum populations and commitment to expansion and differentiation. Using pull-down assays and network analyses, we identified novel SLAMF7-binding intracellular signaling molecules including the CRK, CRKL, and Nck adaptors, which are involved in T-cell contact formation and may mediate SLAMF7 functions in sensing and adhesion. Hence, providing SLAMF7 signals during antigen recognition of CD8+ T cells enhanced their overall magnitude, particularly in responses towards low-affinity antigens, resulting in a significant boost in their proliferation and cytotoxic capacity. Overall, we have identified and characterized a potent initiator of the cytotoxic T lymphocyte response program and revealed advanced mechanisms to improve CD8+ T-cell response decisions against weak viral or tumor-associated antigens, thereby strengthening our defense against such adversaries.

CD8+ T 细胞反应是由细胞间受体与配体相互作用调节的精心安排的过程。这些相互作用关键性地控制着 CD8+ T 细胞群的动态,这对克服病毒感染或癌症等威胁至关重要。然而,这些动态机制仍未完全阐明。在这里,我们发现了 CD8+ T 细胞上的自锁表面受体 SLAMF7(CD319)在细胞毒性 T 细胞反应启动过程中的一种迄今未知的 T 细胞转介功能。根据其在 T 效应细胞上与细胞毒性相关的表达,我们发现 CD8+ T 细胞可利用 SLAMF7 将环境线索转化为细胞相互作用和信息交换。事实上,SLAMF7 可促进形成剂量依赖性的稳定同型接触,最终形成稳定的细胞接触、法定人数群以及扩增和分化承诺。通过牵引试验和网络分析,我们发现了新型 SLAMF7 结合的细胞内信号分子,包括 CRK、CRKL 和 Nck 适配体,它们参与了 T 细胞接触的形成,并可能介导 SLAMF7 在传感和粘附方面的功能。因此,在 CD8+ T 细胞识别抗原的过程中提供 SLAMF7 信号会增强它们的整体数量,尤其是对低亲和力抗原的反应,从而显著提高它们的增殖和细胞毒性能力。总之,我们发现并鉴定了细胞毒性 T 淋巴细胞反应程序的强效启动因子,揭示了改善 CD8+ T 细胞对弱病毒或肿瘤相关抗原反应决策的先进机制,从而加强了我们对此类对手的防御能力。
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引用次数: 0
Activating the NFE2L1-ubiquitin-proteasome system by DDI2 protects from ferroptosis. DDI2激活NFE2L1-泛素-蛋白酶体系统可防止铁变态反应。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-09 DOI: 10.1038/s41418-024-01398-z
Anahita Ofoghi, Stefan Kotschi, Imke L Lemmer, Daniel T Haas, Nienke Willemsen, Batoul Bayer, Anna S Jung, Sophie Möller, Stefanie Haberecht-Müller, Elke Krüger, Natalie Krahmer, Alexander Bartelt

Ferroptosis is an iron-dependent, non-apoptotic form of cell death initiated by oxidative stress and lipid peroxidation. Recent evidence has linked ferroptosis to the action of the transcription factor Nuclear factor erythroid-2 derived,-like-1 (NFE2L1). NFE2L1 regulates proteasome abundance in an adaptive fashion, maintaining protein quality control to secure cellular homeostasis, but the regulation of NFE2L1 during ferroptosis and the role of the ubiquitin-proteasome system (UPS) herein are still unclear. In the present study, using an unbiased proteomic approach charting the specific ubiquitylation sites, we show that induction of ferroptosis leads to recalibration of the UPS. RSL3-induced ferroptosis inhibits proteasome activity and leads to global hyperubiquitylation, which is linked to NFE2L1 activation. As NFE2L1 resides in the endoplasmic reticulum tethered to the membrane, it undergoes complex posttranslational modification steps to become active and induce the expression of proteasome subunit genes. We show that proteolytic cleavage of NFE2L1 by the aspartyl protease DNA-damage inducible 1 homolog 2 (DDI2) is a critical step for the ferroptosis-induced feed-back loop of proteasome function. Cells lacking DDI2 cannot activate NFE2L1 in response to RSL3 and show global hyperubiquitylation. Genetic or chemical induction of ferroptosis in cells with a disrupted DDI2-NFE2L1 pathway diminishes proteasomal activity and promotes cell death. Also, treating cells with the clinical drug nelfinavir, which inhibits DDI2, sensitized cells to ferroptosis. In conclusion, our results provide new insight into the importance of the UPS in ferroptosis and highlight the role of the DDI2-NFE2L1 as a potential therapeutic target. Manipulating DDI2-NFE2L1 activity through chemical inhibition might help sensitizing cells to ferroptosis, thus enhancing existing cancer therapies.

铁凋亡是一种由氧化应激和脂质过氧化引发的铁依赖性、非凋亡性细胞死亡形式。最近的证据表明,铁凋亡与转录因子核因子红细胞-2衍生样-1(NFE2L1)的作用有关。NFE2L1 以适应性方式调节蛋白酶体的丰度,维持蛋白质质量控制以确保细胞稳态,但 NFE2L1 在铁变态反应过程中的调节作用以及泛素-蛋白酶体系统(UPS)在其中的作用仍不清楚。在本研究中,我们采用无偏见的蛋白质组学方法绘制了特定泛素化位点图,结果表明诱导铁变态反应会导致 UPS 的重新校准。RSL3 诱导的铁变态反应抑制了蛋白酶体的活性,导致全局泛素化过度,而泛素化过度与 NFE2L1 的激活有关。由于 NFE2L1 位于内质网中并与膜相连,因此它需要经过复杂的翻译后修饰步骤才能变得活跃并诱导蛋白酶体亚基基因的表达。我们的研究表明,天冬氨酰蛋白酶 DNA-damage inducible 1 homolog 2(DDI2)对 NFE2L1 的蛋白水解是铁变态反应诱导蛋白酶体功能回馈环的关键步骤。缺乏 DDI2 的细胞不能激活 NFE2L1 对 RSL3 作出反应,并表现出整体泛素化过度。在 DDI2-NFE2L1 通路被破坏的细胞中,遗传或化学诱导的铁突变会降低蛋白酶体的活性并促进细胞死亡。此外,用抑制 DDI2 的临床药物奈非那韦处理细胞,也会使细胞对铁蛋白沉积敏感。总之,我们的研究结果为了解 UPS 在铁蛋白沉积过程中的重要性提供了新的视角,并突出了 DDI2-NFE2L1 作为潜在治疗靶点的作用。通过化学抑制操纵 DDI2-NFE2L1 的活性可能有助于使细胞对铁变态反应敏感,从而增强现有的癌症疗法。
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引用次数: 0
A novel glucose sensor fuelling cancer growth 助长癌症生长的新型葡萄糖传感器
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-08 DOI: 10.1038/s41418-024-01400-8
Luisa Ricci, Simone Cardaci
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引用次数: 0
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Cell Death and Differentiation
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