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Metabolic convergence on lipogenesis in RAS, BCR-ABL, and MYC-driven lymphoid malignancies. RAS、BCR-ABL 和 MYC 驱动的淋巴恶性肿瘤中脂肪生成的代谢趋同。
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-08-16 DOI: 10.1186/s40170-021-00263-8
Daniel F Liefwalker, Meital Ryan, Zhichao Wang, Khyatiben V Pathak, Seema Plaisier, Vidhi Shah, Bobby Babra, Gabrielle S Dewson, Ian K Lai, Adriane R Mosley, Patrick T Fueger, Stephanie C Casey, Lei Jiang, Patrick Pirrotte, Srividya Swaminathan, Rosalie C Sears

Background: Metabolic reprogramming is a central feature in many cancer subtypes and a hallmark of cancer. Many therapeutic strategies attempt to exploit this feature, often having unintended side effects on normal metabolic programs and limited efficacy due to integrative nature of metabolic substrate sourcing. Although the initiating oncogenic lesion may vary, tumor cells in lymphoid malignancies often share similar environments and potentially similar metabolic profiles. We examined cells from mouse models of MYC-, RAS-, and BCR-ABL-driven lymphoid malignancies and find a convergence on de novo lipogenesis. We explore the potential role of MYC in mediating lipogenesis by 13C glucose tracing and untargeted metabolic profiling. Inhibition of lipogenesis leads to cell death both in vitro and in vivo and does not induce cell death of normal splenocytes.

Methods: We analyzed RNA-seq data sets for common metabolic convergence in lymphoma and leukemia. Using in vitro cell lines derived in from conditional MYC, RAS, and BCR-ABL transgenic murine models and oncogene-driven human cell lines, we determined gene regulation, metabolic profiles, and sensitivity to inhibition of lipogenesis in lymphoid malignancies. We utilize preclinical murine models and transgenic primary model of T-ALL to determine the effect of lipogenesis blockade across BCR-ABL-, RAS-, and c-MYC-driven lymphoid malignancies. Statistical significance was calculated using unpaired t-tests and one-way ANOVA.

Results: This study illustrates that de novo lipid biogenesis is a shared feature of several lymphoma subtypes. Using cell lines derived from conditional MYC, RAS, and BCR-ABL transgenic murine models, we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(tetradecloxy)-2-furic acid (TOFA), and other lipogenesis inhibitors. We performed metabolic tracing studies to confirm the influence of c-MYC and TOFA on lipogenesis. We identify specific cell death responses to TOFA in vitro and in vivo and demonstrate delayed engraftment and progression in vivo in transplanted lymphoma cell lines. We also observe delayed progression of T-ALL in a primary transgenic mouse model upon TOFA administration. In a panel of human cell lines, we demonstrate sensitivity to TOFA treatment as a metabolic liability due to the general convergence on de novo lipogenesis in lymphoid malignancies driven by MYC, RAS, or BCR-ABL. Importantly, cell death was not significantly observed in non-malignant cells in vivo.

Conclusions: These studies suggest that de novo lipogenesis may be a common survival strategy for many lymphoid malignancies and may be a clinically exploitable metabolic liability.

Trial registration: This study does not include any clinical interventions on human subjects.

背景:代谢重编程是许多癌症亚型的核心特征,也是癌症的标志。许多治疗策略都试图利用这一特点,但往往会对正常代谢程序产生意想不到的副作用,而且由于代谢底物来源的综合性,疗效有限。虽然致癌病灶可能各不相同,但淋巴恶性肿瘤的肿瘤细胞往往具有相似的环境和潜在的相似代谢特征。我们对 MYC、RAS 和 BCR-ABL 驱动的淋巴恶性肿瘤小鼠模型的细胞进行了研究,发现它们在新生脂肪生成方面存在趋同性。我们通过 13C 葡萄糖追踪和非靶向代谢分析,探讨了 MYC 在介导脂肪生成中的潜在作用。抑制脂肪生成会导致体外和体内细胞死亡,但不会诱导正常脾细胞死亡:我们分析了 RNA-seq 数据集,以寻找淋巴瘤和白血病的共同代谢趋同点。利用从条件性 MYC、RAS 和 BCR-ABL 转基因小鼠模型和癌基因驱动的人类细胞系中提取的体外细胞系,我们确定了淋巴恶性肿瘤的基因调控、代谢特征以及对抑制脂肪生成的敏感性。我们利用临床前小鼠模型和 T-ALL 的转基因原代模型来确定阻断脂肪生成对 BCR-ABL、RAS 和 c-MYC 驱动的淋巴恶性肿瘤的影响。采用非配对t检验和单因素方差分析计算统计意义:这项研究表明,新的脂质生物生成是几种淋巴瘤亚型的共同特征。利用从条件性MYC、RAS和BCR-ABL转基因小鼠模型中提取的细胞系,我们证明了乙酰-CoA羧化酶抑制剂5-(十四烷氧基)-2-呋喃酸(TOFA)和其他脂肪生成抑制剂抑制脂肪生成的共同反应。我们进行了代谢追踪研究,以确认 c-MYC 和 TOFA 对脂肪生成的影响。我们确定了体外和体内细胞对 TOFA 的特异性死亡反应,并证明了移植淋巴瘤细胞系在体内的移植和进展延迟。我们还在原代转基因小鼠模型中观察到,服用 TOFA 后,T-ALL 的进展延迟。在一组人类细胞系中,我们证明了对 TOFA 治疗的敏感性,这是由于 MYC、RAS 或 BCR-ABL 驱动的淋巴恶性肿瘤普遍趋向于新生脂肪生成的代谢责任。重要的是,在体内非恶性细胞中没有观察到明显的细胞死亡现象:这些研究表明,新生脂肪生成可能是许多淋巴恶性肿瘤的常见生存策略,也可能是临床上可利用的代谢责任:本研究不包括对人体的任何临床干预。
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引用次数: 1
礫浜性マメアカイソガニ(モクズガニ科)の能登半島と九州沿岸からの記録 来自能登半岛和九州沿岸的砾滨性赤红蟹(木蟹科)记录
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-08-01 DOI: 10.18988/CANCER.30.0_49
中岡 由起子, 恵次 和田
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引用次数: 0
日本初記録の2種を含む琉球列島産のヒラベニオウギガニ属(十脚目:短尾下目:オウギガニ科) 琉球列岛产的平口蟹属(十足目:短尾下目:平口蟹科),包括日本首次记录的两种。
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-08-01 DOI: 10.18988/CANCER.30.0_73
唯史 前之園
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引用次数: 0
日本初記録種を含む琉球列島産のシンオウギガニ亜科(甲殻亜門:十脚目:短尾下目:オウギガニ科) 日本首次记录的琉球列岛产新扇蟹亚科(甲壳亚门:足目:短尾下目:扇蟹科)
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-08-01 DOI: 10.18988/CANCER.30.0_21
唯史 前之園
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引用次数: 0
八重山諸島小浜島より記録されたヤエヤマヤマガニ(甲殻亜門:十脚目:短尾下目:サワガニ科) 八重山诸岛小滨岛记录的八重山蟹(甲壳亚门:足足目:短尾下目:小蟹科)
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-08-01 DOI: 10.18988/CANCER.30.0_11
喜久 藤田, 智史 佐伯, 将一 仲吉, 新 福島, 貫 成瀬
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引用次数: 0
Impaired anaplerosis is a major contributor to glycolysis inhibitor toxicity in glioma. 神经胶质瘤中糖酵解抑制剂毒性的一个主要因素是硬化受损。
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-06-25 DOI: 10.1186/s40170-021-00259-4
Sunada Khadka, Kenisha Arthur, Yasaman Barekatain, Eliot Behr, Mykia Washington, Jeffrey Ackroyd, Kaitlyn Crowley, Pornpa Suriyamongkol, Yu-Hsi Lin, Cong-Dat Pham, Rafal Zielinski, Marissa Trujillo, James Galligan, Dimitra K Georgiou, John Asara, Florian Muller

Background: Reprogramming of metabolic pathways is crucial to satisfy the bioenergetic and biosynthetic demands and maintain the redox status of rapidly proliferating cancer cells. In tumors, the tricarboxylic acid (TCA) cycle generates biosynthetic intermediates and must be replenished (anaplerosis), mainly from pyruvate and glutamine. We recently described a novel enolase inhibitor, HEX, and its pro-drug POMHEX. Since glycolysis inhibition would deprive the cell of a key source of pyruvate, we hypothesized that enolase inhibitors might inhibit anaplerosis and synergize with other inhibitors of anaplerosis, such as the glutaminase inhibitor, CB-839.

Methods: We analyzed polar metabolites in sensitive (ENO1-deleted) and resistant (ENO1-WT) glioma cells treated with enolase and glutaminase inhibitors. We investigated whether sensitivity to enolase inhibitors could be attenuated by exogenous anaplerotic metabolites. We also determined the synergy between enolase inhibitors and the glutaminase inhibitor CB-839 in glioma cells in vitro and in vivo in both intracranial and subcutaneous tumor models.

Results: Metabolomic profiling of ENO1-deleted glioma cells treated with the enolase inhibitor revealed a profound decrease in the TCA cycle metabolites with the toxicity reversible upon exogenous supplementation of supraphysiological levels of anaplerotic substrates, including pyruvate. ENO1-deleted cells also exhibited selective sensitivity to the glutaminase inhibitor CB-839, in a manner rescuable by supplementation of anaplerotic substrates or plasma-like media PlasmaxTM. In vitro, the interaction of these two drugs yielded a strong synergistic interaction but the antineoplastic effects of CB-839 as a single agent in ENO1-deleted xenograft tumors in vivo were modest in both intracranial orthotopic tumors, where the limited efficacy could be attributed to the blood-brain barrier (BBB), and subcutaneous xenografts, where BBB penetration is not an issue. This contrasts with the enolase inhibitor HEX, which, despite its negative charge, achieved antineoplastic effects in both intracranial and subcutaneous tumors.

Conclusion: Together, these data suggest that at least for ENO1-deleted gliomas, tumors in vivo-unlike cells in culture-show limited dependence on glutaminolysis and instead primarily depend on glycolysis for anaplerosis. Our findings reinforce the previously reported metabolic idiosyncrasies of in vitro culture and suggest that cell culture media nutrient composition more faithful to the in vivo environment will more accurately predict in vivo efficacy of metabolism targeting drugs.

背景:代谢途径的重编程对于满足快速增殖的癌细胞的生物能量和生物合成需求以及维持氧化还原状态至关重要。在肿瘤中,三羧酸(TCA)循环产生生物合成中间体,必须主要从丙酮酸和谷氨酰胺中补充(过敏)。我们最近描述了一种新型烯醇化酶抑制剂HEX及其前药POMHEX。由于糖酵解抑制会剥夺细胞中丙酮酸的关键来源,我们假设烯醇化酶抑制剂可能抑制过敏反应,并与其他过敏反应抑制剂协同作用,如谷氨酰胺酶抑制剂CB-839。方法:我们分析了烯醇化酶和谷氨酰胺酶抑制剂处理的敏感(eno1缺失)和耐药(eno1 wt)胶质瘤细胞的极性代谢物。我们研究了外源性的折叠性代谢物是否可以减弱对烯醇化酶抑制剂的敏感性。我们还确定了烯醇化酶抑制剂和谷氨酰胺酶抑制剂CB-839在颅内和皮下肿瘤模型中体外和体内胶质瘤细胞中的协同作用。结果:用烯醇化酶抑制剂处理的eno1缺失胶质瘤细胞的代谢组学分析显示,TCA循环代谢物的显著减少,并且在外源性补充超生理水平的反折叠底物(包括丙酮酸)后,毒性可逆。eno1缺失的细胞也表现出对谷氨酰胺酶抑制剂CB-839的选择性敏感性,这种敏感性可以通过补充复变底物或血浆样培养基PlasmaxTM来修复。在体外,这两种药物的相互作用产生了很强的协同相互作用,但CB-839作为单一药物在体内对eno1缺失的异种移植物肿瘤的抗肿瘤作用一般,在颅内原位肿瘤中,有限的疗效可能是由于血脑屏障(BBB),而皮下异种移植物,在血脑屏障穿透方面没有问题。这与烯醇化酶抑制剂HEX形成对比,后者尽管带负电荷,但在颅内和皮下肿瘤中均具有抗肿瘤作用。结论:综上所述,这些数据表明,至少对于eno1缺失的胶质瘤,与培养细胞不同,体内肿瘤对谷氨酰胺酶解的依赖性有限,而主要依赖糖酵解来治疗骨质疏松。我们的研究结果加强了先前报道的体外培养的代谢特性,并表明更忠于体内环境的细胞培养基营养成分将更准确地预测代谢靶向药物的体内疗效。
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引用次数: 11
Index 指数
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-01-01 DOI: 10.1016/b978-0-12-819547-5.09999-5
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引用次数: 0
Oxidative stress in lung cancer 肺癌中的氧化应激
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-01-01 DOI: 10.1016/B978-0-12-405205-5.00003-9
W. Loke, Mann Ying Lim, C. Lewis, P. Thomas
{"title":"Oxidative stress in lung cancer","authors":"W. Loke, Mann Ying Lim, C. Lewis, P. Thomas","doi":"10.1016/B978-0-12-405205-5.00003-9","DOIUrl":"https://doi.org/10.1016/B978-0-12-405205-5.00003-9","url":null,"abstract":"","PeriodicalId":9418,"journal":{"name":"Cancer & Metabolism","volume":"09 1","pages":""},"PeriodicalIF":5.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86503135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Fern extract, oxidative stress, and skin cancer 蕨类植物提取物,氧化应激和皮肤癌
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-01-01 DOI: 10.1016/B978-0-12-405205-5.00025-8
C. Parrado, Á. Juarranz, Y. Gilaberte, N. Philips, S. González
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引用次数: 4
Curcumin analogs, oxidative stress, and prostate cancer 姜黄素类似物,氧化应激和前列腺癌
IF 5.9 3区 医学 Q1 CELL BIOLOGY Pub Date : 2021-01-01 DOI: 10.1016/B978-0-12-405205-5.00018-0
Alexandra M. Fajardo, M. Bisoffi
{"title":"Curcumin analogs, oxidative stress, and prostate cancer","authors":"Alexandra M. Fajardo, M. Bisoffi","doi":"10.1016/B978-0-12-405205-5.00018-0","DOIUrl":"https://doi.org/10.1016/B978-0-12-405205-5.00018-0","url":null,"abstract":"","PeriodicalId":9418,"journal":{"name":"Cancer & Metabolism","volume":"37 1","pages":""},"PeriodicalIF":5.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87530549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
期刊
Cancer & Metabolism
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