Research Papers:

Increased gene expression noise in human cancers is correlated with low p53 and immune activities as well as late stage cancer

Rongfei Han, Guanqun Huang, Yejun Wang, Yafei Xu, Yueming Hu, Wenqi Jiang, Tianfu Wang, Tian Xiao and Duo Zheng _

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Oncotarget. 2016; 7:72011-72020. https://doi.org/10.18632/oncotarget.12457

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Rongfei Han1,*, Guanqun Huang1,*, Yejun Wang1, Yafei Xu1, Yueming Hu1, Wenqi Jiang1, Tianfu Wang2, Tian Xiao1, Duo Zheng1

1Shenzhen Key Laboratory of Translational Medicine of Tumor, Department of Cell Biology and Genetics, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, 518060, P.R.China

2Guangdong Key Laboratory for Biomedical Measurements and Ultrasound Imaging, School of Biomedical Engineering, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, 518060, P.R.China

*These authors contributed equally to this work

Correspondence to:

Tianfu Wang, email: [email protected]

Tian Xiao, email: [email protected]

Duo Zheng, email: [email protected]

Keywords: gene expression noise, p53, immune activity, cancer prognosis

Received: July 26, 2016     Accepted: September 29, 2016     Published: October 04, 2016


Gene expression in metazoans is delicately organized. As genetic information transmits from DNA to RNA and protein, expression noise is inevitably generated. Recent studies begin to unveil the mechanisms of gene expression noise control, but the changes of gene expression precision in pathologic conditions like cancers are unknown. Here we analyzed the transcriptomic data of human breast, liver, lung and colon cancers, and found that the expression noise of more than 74.9% genes was increased in cancer tissues as compared to adjacent normal tissues. This suggested that gene expression precision controlling collapsed during cancer development. A set of 269 genes with noise increased more than 2-fold were identified across different cancer types. These genes were involved in cell adhesion, catalytic and metabolic functions, implying the vulnerability of deregulation of these processes in cancers. We also observed a tendency of increased expression noise in patients with low p53 and immune activity in breast, liver and lung caners but not in colon cancers, which indicated the contributions of p53 signaling and host immune surveillance to gene expression noise in cancers. Moreover, more than 53.7% genes had increased noise in patients with late stage than early stage cancers, suggesting that gene expression precision was associated with cancer outcome. Together, these results provided genomic scale explorations of gene expression noise control in human cancers.

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