LncRNA REG1CP promotes tumorigenesis through an enhancer complex to recruit FANCJ helicase for REG3A transcription

Hamed Yari, Lei Jin, Liu Teng, Yufang Wang, Yongyan Wu, Guang Zhi Liu, Wei Gao, Jin Liang, Yanfeng Xi, Yu Chen Feng, Chunming Zhang, Yuan Yuan Zhang, Hessam Tabatabaee, Ting La, Rui Hong Yang, Fu Hua Wang, Xu Guang Yan, Margaret Farrelly, Rodney Scott, Tao Liu, Rick F. Thorne, Su Tang Guo () and Xu Dong Zhang ()
Additional contact information
Hamed Yari: The University of Newcastle
Lei Jin: The University of Newcastle
Liu Teng: Zhengzhou University
Yufang Wang: Sichuan University
Yongyan Wu: Shanxi Medical University
Guang Zhi Liu: Zhengzhou University
Wei Gao: Shanxi Medical University
Jin Liang: Shanxi Medical University
Yanfeng Xi: Shanxi Medical University
Yu Chen Feng: The University of Newcastle
Chunming Zhang: Shanxi Medical University
Yuan Yuan Zhang: The University of Newcastle
Hessam Tabatabaee: The University of Newcastle
Ting La: The University of Newcastle
Rui Hong Yang: Shanxi Medical University
Fu Hua Wang: Shanxi Medical University
Xu Guang Yan: The University of Newcastle
Margaret Farrelly: The University of Newcastle
Rodney Scott: The University of Newcastle
Tao Liu: University of New South Wales
Rick F. Thorne: The University of Newcastle
Su Tang Guo: Shanxi Medical University
Xu Dong Zhang: The University of Newcastle

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract Protein products of the regenerating islet-derived (REG) gene family are important regulators of many cellular processes. Here we functionally characterise a non-protein coding product of the family, the long noncoding RNA (lncRNA) REG1CP that is transcribed from a DNA fragment at the family locus previously thought to be a pseudogene. REG1CP forms an RNA–DNA triplex with a homopurine stretch at the distal promoter of the REG3A gene, through which the DNA helicase FANCJ is tethered to the core promoter of REG3A where it unwinds double stranded DNA and facilitates a permissive state for glucocorticoid receptor α (GRα)-mediated REG3A transcription. As such, REG1CP promotes cancer cell proliferation and tumorigenicity and its upregulation is associated with poor outcome of patients. REG1CP is also transcriptionally inducible by GRα, indicative of feedforward regulation. These results reveal the function and regulation of REG1CP and suggest that REG1CP may constitute a target for cancer treatment.

Date: 2019
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DOI: 10.1038/s41467-019-13313-z

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