A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy

Canne Ian G.; Merrick Karl A.; Morandell Sandra; Zhu Chang-Qi; Braun Christian J.; Grant Robert A.; Cameron Eleanor R.; Tsao Ming-Sound; Hemann Michael T.; Yaffe Michael B.

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A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy

机译：多效性RNA结合蛋白控制不同的细胞周期检查点，以驱动p53缺陷型肿瘤对化疗的耐药性。

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In normal cells, p53 is activated by DNA damage checkpoint kinases to simultaneously control the G1/S and G2/M cell cycle checkpoints through transcriptional induction of p21(cip1) and Gadd45 alpha. In p53-mutant tumors, cell cycle checkpoints are rewired, leading to dependency on the p38/MK2 pathway to survive DNA-damaging chemotherapy. Here we show that the RNA binding protein hnRNPA0 is the "successor" to p53 for checkpoint control. Like p53, hnRNPA0 is activated by a checkpoint kinase (MK2) and simultaneously controls both cell cycle checkpoints through distinct target mRNAs, but unlike p53, this is through the post-transcriptional stabilization of p27(Kip1) and Gadd45 alpha mRNAs. This pathway drives cisplatin resistance in lung cancer, demonstrating the importance of post-transcriptional RNA control to chemotherapy response.

机译：在正常细胞中，p53被DNA损伤检查点激酶激活，以通过转录诱导p21（cip1）和Gadd45 alpha来同时控制G1 / S和G2 / M细胞周期检查点。在p53突变的肿瘤中，细胞周期检查点被重新连接，导致依赖p38 / MK2途径来生存破坏DNA的化学疗法。在这里，我们显示RNA结合蛋白hnRNPA0是p53用于检查点控制的“后继者”。像p53一样，hnRNPA0被检查点激酶（MK2）激活，并通过不同的靶mRNA同时控制两个细胞周期检查点，但与p53不同，这是通过p27（Kip1）和Gadd45 alpha mRNA的转录后稳定作用。该途径驱动肺癌中的顺铂耐药性，证明转录后RNA控制对化学疗法反应的重要性。

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《Cancer Cell》 |2015年第5期|共15页
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Canne Ian G.; Merrick Karl A.; Morandell Sandra; Zhu Chang-Qi; Braun Christian J.; Grant Robert A.; Cameron Eleanor R.; Tsao Ming-Sound; Hemann Michael T.; Yaffe Michael B.;
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正文语种 eng
中图分类肿瘤学;
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1. A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy [J] . Canne Ian G., Merrick Karl A., Morandell Sandra, Cancer Cell . 2015,第5期

机译：多效性RNA结合蛋白控制不同的细胞周期检查点，以驱动p53缺陷型肿瘤对化疗的耐药性。
2. Acetylation of MORC2 by NAT10 regulates cell-cycle checkpoint control and resistance to DNA-damaging chemotherapy and radiotherapy in breast cancer [J] . Liu Hong-Yi, Liu Ying-Ying, Yang Fan, Nucleic Acids Research . 2020,第7期

机译：NAT10的Morc2乙酰化调节细胞周期检查点控制和对乳腺癌的DNA损伤化疗和放射疗法的抗性
3. Acetylation of MORC2 by NAT10 regulates cell-cycle checkpoint control and resistance to DNA-damaging chemotherapy and radiotherapy in breast cancer [J] . Hong-Yi Liu, Ying-Ying Liu, Fan Yang, Nucleic acids research . 2020,第7期

机译：NAT10的Morc2乙酰化调节细胞周期检查点控制和对乳腺癌的DNA损伤化疗和放射疗法的抗性
4. Overcoming therapeutic resistance in pancreatic cancer is not a simple mix of PDT and chemotherapy: Evaluation of PDT-chemotherapy combinations in 3D tumor models [C] . Jonathan P. Celli, Ljubica Petrovic, Iqbal Massodi, Optical methods for tumor treatment and detection: mechanisms and techniques in photodynamic therapy XXII . 2013

机译：克服胰腺癌的治疗抗性不是PDT和化学疗法的简单组合：在3D肿瘤模型中评估PDT-化学疗法的组合
5. Cell cycle inhibition as a mode of abnormal development: The role of cell cycle checkpoint proteins and cyclin-dependent kinase inhibitors in neurodevelopmental toxicant defense. [D] . Gribble, Elizabeth J. 2005

机译：细胞周期抑制是异常发育的一种方式：细胞周期检查点蛋白和细胞周期蛋白依赖性激酶抑制剂在神经发育毒物防御中的作用。
6. A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-defective Tumors to Chemotherapy [O] . Ian G Cannell, Karl A Merrick, Sandra Morandell, -1

机译：多效性RNA结合蛋白控制不同的细胞周期检查点以驱动p53缺陷肿瘤对化疗的耐药性。
7. A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy [O] . Cannell Ian G., Merrick Karl A., Morandell Sandra, 2015

机译：多效性RNA结合蛋白控制不同的细胞周期检查点，以驱动p53缺陷肿瘤对化疗的耐药性。

A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy

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