Genome-wide transcriptome profiling of homologous recombination DNA repair

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 and Shiaw-Yih Lin ()
Additional contact information
Guang Peng: Unit 1013, The University of Texas MD Anderson Cancer Center
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

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4361

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