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Genome-wide transcriptome profiling of homologous recombination DNA repair

Author

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  • Guang Peng

    (Unit 1013, The University of Texas MD Anderson Cancer Center
    Tongji Hospital, Tongji Medical College, The University of Huazhong Science & Technology)

  • Curtis Chun-Jen Lin

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Wei Mo

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Hui Dai

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Yun-Yong Park

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Soo Mi Kim

    (Chonbuk National University Medical School)

  • Yang Peng

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Qianxing Mo

    (Dan L. Duncan Cancer Center, Baylor College of Medicine)

  • Stefan Siwko

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Ruozhen Hu

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Ju-Seog Lee

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Bryan Hennessy

    (Centre for Systems Medicine, Royal College of Surgeons in Ireland)

  • Samir Hanash

    (Unit 1013, The University of Texas MD Anderson Cancer Center)

  • Gordon B. Mills

    (Unit 950, The University of Texas MD Anderson Cancer Center)

  • Shiaw-Yih Lin

    (Unit 950, The University of Texas MD Anderson Cancer Center)

Abstract

Homologous recombination (HR) repair deficiency predisposes to cancer development, but also sensitizes cancer cells to DNA damage-inducing therapeutics. Here we identify an HR defect (HRD) gene signature that can be used to functionally assess HR repair status without interrogating individual genetic alterations in cells. By using this HRD gene signature as a functional network analysis tool, we discover that simultaneous loss of two major tumour suppressors BRCA1 and PTEN extensively rewire the HR repair-deficient phenotype, which is found in cells with defects in either BRCA1 or PTEN alone. Moreover, the HRD gene signature serves as an effective drug discovery platform to identify agents targeting HR repair as potential chemo/radio sensitizers. More importantly, this HRD gene signature is able to predict clinical outcomes across multiple cancer lineages. Our findings, therefore, provide a molecular profile of HR repair to assess its status at a functional network level, which can provide both biological insights and have clinical implications in cancer.

Suggested Citation

  • Guang Peng & Curtis Chun-Jen Lin & Wei Mo & Hui Dai & Yun-Yong Park & Soo Mi Kim & Yang Peng & Qianxing Mo & Stefan Siwko & Ruozhen Hu & Ju-Seog Lee & Bryan Hennessy & Samir Hanash & Gordon B. Mills &, 2014. "Genome-wide transcriptome profiling of homologous recombination DNA repair," Nature Communications, Nature, vol. 5(1), pages 1-11, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4361
    DOI: 10.1038/ncomms4361
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    Cited by:

    1. Lei Tao & Yue Zhou & Xiangyu Pan & Yuan Luo & Jiahao Qiu & Xia Zhou & Zhiqian Chen & Yan Li & Lian Xu & Yang Zhou & Zeping Zuo & Chunqi Liu & Liang Wang & Xiaocong Liu & Xinyu Tian & Na Su & Zhengnan , 2023. "Repression of LSD1 potentiates homologous recombination-proficient ovarian cancer to PARP inhibitors through down-regulation of BRCA1/2 and RAD51," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    2. Masoumeh Moslemi & Ehsan Sohrabi & Nemamali Azadi & Ali Zekri & Hamed Afkhami & Mansoor Khaledi & Ehsan Razmara, 2020. "Expression Analysis of EEPD1 and MUS81 Genes in Breast Cancer," Biomedical Journal of Scientific & Technical Research, Biomedical Research Network+, LLC, vol. 29(4), pages 22556-22564, August.
    3. Julia Schöpf & Sebastian Uhrig & Christoph E. Heilig & Kwang-Seok Lee & Tatjana Walther & Alexander Carazzato & Anna Maria Dobberkau & Dieter Weichenhan & Christoph Plass & Mark Hartmann & Gaurav D. D, 2024. "Multi-omic and functional analysis for classification and treatment of sarcomas with FUS-TFCP2 or EWSR1-TFCP2 fusions," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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