MAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer

Augert Arnaud; Mathsyaraja Haritha; Ibrahim Ali H.; Freie Brian; Geuenich Michael J.; Cheng Pei-Feng; Alibeckoff Sydney P.; Wu Nan; Hiatt Joseph B.; Basom Ryan; Gazdar Adi; Sullivan Lucas B.; Eisenman Robert N.; MacPherson David

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MAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer

机译：最大用作肿瘤抑制器和在小细胞肺癌中重新丝代谢

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Small cell lung cancer (SCLC) is a highly aggressive and lethal neoplasm. To identify candidate tumor suppressors we applied CRISPR/Cas9 gene inactivation screens to a cellular model of early-stage SCLC. Among the top hits was MAX, the obligate heterodimerization partner for MYC family proteins that is mutated in human SCLC. Max deletion increases growth and transformation in cells and dramatically accelerates SCLC progression in an Rb1/Trp53-deleted mouse model. In contrast, deletion of Max abrogates tumorigenesis in MYCL-overexpressing SCLC. Max deletion in SCLC resulted in derepression of metabolic genes involved in serine and one-carbon metabolism. By increasing serine biosynthesis, Max-deleted cells exhibit resistance to serine depletion. Thus, Max loss results in metabolic rewiring and context-specific tumor suppression.

机译：小细胞肺癌（SCLC）是一种高度侵袭性和致死性的肿瘤。为了确定候选肿瘤抑制因子，我们将CRISPR/Cas9基因失活筛选应用于早期SCLC的细胞模型。其中最受欢迎的是MAX，它是MYC家族蛋白的专性异二聚体伴侣，在人类SCLC中发生突变。在Rb1/Trp53缺失的小鼠模型中，Max缺失可增加细胞的生长和转化，并显著加速SCLC的进展。相反，在MYCL过度表达的SCLC中，删除Max可消除肿瘤发生。SCLC中的Max缺失导致参与丝氨酸和单碳代谢的代谢基因表达降低。通过增加丝氨酸生物合成，最大缺失细胞表现出对丝氨酸消耗的抵抗力。因此，最大损失导致代谢重组和环境特异性肿瘤抑制。

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《Cancer Cell》 |2020年第1期|共25页
作者
Augert Arnaud; Mathsyaraja Haritha; Ibrahim Ali H.; Freie Brian; Geuenich Michael J.; Cheng Pei-Feng; Alibeckoff Sydney P.; Wu Nan; Hiatt Joseph B.; Basom Ryan; Gazdar Adi; Sullivan Lucas B.; Eisenman Robert N.; MacPherson David;
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Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Basic Sci Div Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Basic Sci Div Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Basic Sci Div Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Basic Sci Div Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Genom &

Bioinformat Shared Resource 1100 Fairview Ave N Seattle WA;

Univ Texas SouthWestern 6000 Harry Hines Blvd Dallas TX 75235 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Basic Sci Div Seattle WA 98109 USA;

Fred Hutchinson Canc Res Ctr Div Human Biol 1100 Fairview Ave N Seattle WA 98109 USA;

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正文语种 eng
中图分类肿瘤学;
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专利

1. VGLL4 functions as a new tumor suppressor in lung cancer by negatively regulating the YAP-TEAD transcriptional complex [J] . Wenjing Zhang, Yijun Gao, Peixue Li, 细胞研究（英文版） . 2014,第003期
2. FOXA2 functions as a suppressor of tumor metastasis by inhibition of epithelial-to-mesenchymal transition in human lung cancers [J] . Yunneng Tang, Guangwen Shu, Xinwang Yuan, 细胞研究：英文版 . 2011,第002期
3. FOXA2 functions as a suppressor of tumor metastasis by inhibition of epithelial-to-mesenchymal transition in human lung cancers [J] . Yunneng Tang, Guangwen Shu, Xinwang Yuan, 细胞研究（英文版） . 2011,第002期
4. Somatic and germline mutations in the tumor suppressor gene PARK2 impair PINK1/Parkin-mediated mitophagy in lung cancer cells [J] . Zeng-li Zhang, Zheng Ying, Na-na Wang, 中国药理学报：英文版 . 2020,第001期
5. MAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer [J] . Augert Arnaud, Mathsyaraja Haritha, Ibrahim Ali H., Ecological restoration . 2020,第1期

机译：最大用作肿瘤抑制器和在小细胞肺癌中重新丝代谢
6. Tumor suppressor in lung cancer 1 (TSLC1), a novel tumor suppressor gene, is implicated in the regulation of proliferation, invasion, cell cycle, apoptosis, and tumorigenicity in cutaneous squamous cell carcinoma [J] . LiuD., FengX., WuX., Tumour biology : . 2013,第6期

机译：肺癌1（TSLC1）的肿瘤抑制基因是一种新型的肿瘤抑制基因，与皮肤鳞状细胞癌的增殖，侵袭，细胞周期，细胞凋亡和致瘤性有关。
7. MicroRNA-374b-5p Functions as a Tumor Suppressor in Non-Small Cell Lung Cancer by Targeting FOXP1 and Predicts Prognosis of Cancer Patients [J] . Jianzhao Li, Xinfang Zhang, Jiaying Tang, OncoTargets and therapy . 2020,第2期

机译：MicroRNA-374B-5P通过靶向Foxp1并预测癌症患者的预后，用作非小细胞肺癌中的肿瘤抑制剂
8. A Mechanistic Study of IncRNA Fendrr Regulation of FoxF1 Lung Cancer Tumor Suppressor [C] . Carmen Navarro, Carlos Cano, Marta Cuadros, International Work-Conference on Bioinformatics and Biomedical Engineering . 2016

机译：FoxF1肺癌肿瘤抑制器IncRNA Fendrr调控的机制研究
9. The delivery of the FHIT tumor suppressor protein into lung cancer cells. [D] . Gunn, Laura. 2003

机译：FHIT抑癌蛋白向肺癌细胞的递送。
10. Biophysical characterization of the b-HLH-LZ of ΔMax, an alternatively spliced isoform of Max found in tumor cells: Towards the validation of a tumor suppressor role for the Max homodimers [O] . Loïka Maltais, Martin Montagne, Mikaël Bédard, 2012

机译：在肿瘤细胞中发现的Max的另一种剪接异构体ΔMax的b-HLH-LZ的生物物理特性：验证Max同源二聚体的抑癌作用
11. miR-27a-3p Functions as a Tumor Suppressor and Regulates Non-Small Cell Lung Cancer Cell Proliferation via Targeting HOXB8 [O] . Xiaohong Yan, Hui Yu, Yao Liu, 2019

机译：miR-27a-3p作为肿瘤抑制剂，通过靶向hoxb8调节非小细胞肺癌细胞增殖
12. Role of CDK5 as a Tumor Suppressor Gene in Non-Small Cell Lung Cancer. [R] . Nelkin, B. D. 2014

机译：CDK5在非小细胞肺癌中作为肿瘤抑制基因的作用。

MAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer

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