ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma

Marchesini Matteo; Ogoti Yamini; Fiorini Elena; Samur Anil Aktas; Nezi Luigi; DAnca Marianna; Storti Paola; Samur Mehmet Kemal; Ganan-Gomez Irene; Fulciniti Maria Teresa; Mistry Nipun; Jiang Shan; Bao Naran; Marchica Valentina; Neri Antonino; Bueso-Ramos Carlos; Wu Chang-Jiun; Zhang Li; Liang Han; Peng Xinxin; Giuliani Nicola; Draetta Giulio; Clise-Dwyer Karen; Kantarjian Hagop; Munshi Nikhil; Orlowski Robert; Garcia-Manero Guillermo; DePinho Ronald A.; Colla Simona

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ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma

机译：ILF2是1Q21 - 扩增多发性骨髓瘤的RNA剪接和DNA损伤反应的调节剂

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Amplification of 1q21 occurs in approximately 30% of denovo and 70% of relapsed multiple myeloma(MM) and is correlated with disease progression and drug resistance. Here, we provide evidence that the 1q21 amplification-driven overexpression of ILF2 in MM promotes tolerance of genomic instability and drives resistance to DNA-damaging agents. Mechanistically, elevated ILF2 expression exerts resistance to genotoxic agents by modulating YB-1 nuclear localization and interaction with the splicing factor U2AF65, which promotes mRNA processing and the stabilization of transcripts involved in homologous recombination in response to DNA damage. The intimate link between 1q21-amplified ILF2 and the regulation of RNA splicing of DNA repair genes may be exploited to optimize the use of DNA-damaging agents in patients with high-risk MM.

机译：1Q21的扩增发生在约30％的Denovo和70％的复发多发性骨髓瘤（mm）中，并与疾病进展和耐药性相关。在这里，我们提供了证据表明，ILF2的1Q21扩增驱动过表达ILF2促进基因组不稳定性的耐受性，并驱动对DNA损伤剂的抗性。机械地，通过调节Yb-1核定位和与剪接因子U2AF65的相互作用来施加对遗传毒剂的耐受性对遗传毒剂的抵抗力，这促进了MRNA处理和响应于DNA损伤的同源重组中参与的转录物的稳定性。可以利用1Q21扩增ILF2与DNA修复基因的RNA剪接调节的亲密联系，以优化高风险MM患者的DNA损伤剂的使用。

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来源
《Cancer Cell》 |2017年第1期|共19页
作者
Marchesini Matteo; Ogoti Yamini; Fiorini Elena; Samur Anil Aktas; Nezi Luigi; DAnca Marianna; Storti Paola; Samur Mehmet Kemal; Ganan-Gomez Irene; Fulciniti Maria Teresa; Mistry Nipun; Jiang Shan; Bao Naran; Marchica Valentina; Neri Antonino; Bueso-Ramos Carlos; Wu Chang-Jiun; Zhang Li; Liang Han; Peng Xinxin; Giuliani Nicola; Draetta Giulio; Clise-Dwyer Karen; Kantarjian Hagop; Munshi Nikhil; Orlowski Robert; Garcia-Manero Guillermo; DePinho Ronald A.; Colla Simona;
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作者单位

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Dana Farber Canc Inst Dept Biostat &

Computat Biol Boston MA 02215 USA;

Univ Texas MD Anderson Canc Ctr Dept Genom Med Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Parma Dept Clin &

Expt Med I-43100 Parma Italy;

Dana Farber Canc Inst Dept Biostat &

Computat Biol Boston MA 02215 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Dana Farber Canc Inst LeBow Inst Myeloma Therapeut Boston MA 02215 USA;

Univ Texas MD Anderson Canc Ctr Dept Bioinformat &

Computat Biol Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Parma Dept Clin &

Expt Med I-43100 Parma Italy;

Univ Milan Dept Oncol &

Hematooncol I-20122 Milan Italy;

Univ Texas MD Canc Ctr Dept Hematopathol Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Genom Med Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Bioinformat &

Computat Biol Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Bioinformat &

Computat Biol Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Bioinformat &

Computat Biol Houston TX 77030 USA;

Univ Parma Dept Clin &

Expt Med I-43100 Parma Italy;

Univ Texas MD Anderson Canc Ctr Dept Genom Med Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Stem Cell Transplantat &

Cellular Therapy Houston TX 77030;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Texas MD Canc Ctr Dept Lymphoma Myeloma Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Canc Biol Houston TX 77030 USA;

Univ Texas MD Anderson Canc Ctr Dept Leukemia Houston TX 77030 USA;

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正文语种 eng
中图分类肿瘤学;
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专利

1. ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma [J] . Marchesini Matteo, Ogoti Yamini, Fiorini Elena, Cancer Cell . 2017,第1期

机译：ILF2是1Q21 - 扩增多发性骨髓瘤的RNA剪接和DNA损伤反应的调节剂
2. Expression of human BRCA1δ17-19 alternative splicing variant with a truncated BRCT domain in MCF-7 cells results in impaired assembly of DNA repair complexes and aberrant DNA damage response [J] . Sevcik J., Falk M., Macurek L., Cellular Signalling . 2013,第5期

机译：具有截短的BRCT结构域的人BRCA1δ17-19选择性剪接变体在MCF-7细胞中的表达导致DNA修复复合物的装配受损和异常的DNA损伤反应
3. The RNA processing factors THRAP3 and BCLAF1 promote the DNA damage response through selective mRNA splicing and nuclear export [J] . Vohhodina Jekaterina, Barros Eliana M., Savage Abigail L., Nucleic Acids Research . 2017,第22期

机译：RNA处理因子Thrap3和BCLAF1通过选择性mRNA剪接和核出口促进DNA损伤响应
4. Development of a Quantitative SRM Assay for Histone H2AX Ser139 Phosphorylation, a Key Regulator of the DNA Damage Response (DDR) [C] . V Lunyak, A Prakash, M Athanas, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2010

机译：组蛋白H2AX Ser139磷酸化的定量SRM测定，DNA损伤响应的关键调节器（DDR）
5. The Fanconi anemia (FA)/BRCA DNA damage repair pathway is regulated by NF-kappaB and mediates drug resistance in multiple myeloma. [D] . Yarde, Danielle N. 2010

机译：范可尼贫血（FA）/ BRCA DNA损伤修复途径受NF-κB调节并介导多发性骨髓瘤的耐药性。
6. ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma [O] . Matteo Marchesini, Yamini Ogoti, Elena Fiorini, -1

机译：ILF2是1q21扩增的多发性骨髓瘤中RNA剪接和DNA损伤反应的调节剂。
7. ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma [O] . Matteo Marchesini, Yamini Ogoti, Elena Fiorini, 2017

机译：ILF2是1Q21 - 扩增多发性骨髓瘤的RNA剪接和DNA损伤反应的调节剂
8. Understanding Selective Downregulation of c-Myc Expression through Inhibition of General Transcription Regulators in Multiple Myeloma. [R] . Lin, C. 2015

机译：通过抑制多发性骨髓瘤中的一般转录调节因子来了解c-myc表达的选择性下调。

ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma

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