Nature Communications (Sep 2018)
Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression
- Yuan Jiang,
- Yan-Yi Jiang,
- Jian-Jun Xie,
- Anand Mayakonda,
- Masaharu Hazawa,
- Li Chen,
- Jin-Fen Xiao,
- Chun-Quan Li,
- Mo-Li Huang,
- Ling-Wen Ding,
- Qiao-Yang Sun,
- Liang Xu,
- Deepika Kanojia,
- Maya Jeitany,
- Jian-Wen Deng,
- Lian-Di Liao,
- Harmik J. Soukiasian,
- Benjamin P. Berman,
- Jia-Jie Hao,
- Li-Yan Xu,
- En-Min Li,
- Ming-Rong Wang,
- Xin-Gang Bi,
- De-Chen Lin,
- H. Phillip Koeffler
Affiliations
- Yuan Jiang
- Cancer Science Institute of Singapore, National University of Singapore
- Yan-Yi Jiang
- Cancer Science Institute of Singapore, National University of Singapore
- Jian-Jun Xie
- Department of Biochemistry and Molecular Biology, Medical College of Shantou University
- Anand Mayakonda
- Cancer Science Institute of Singapore, National University of Singapore
- Masaharu Hazawa
- Cell-Bionomics Research Unit, Innovative Integrated Bio-Research Core, Institute for Frontier Science Initiative, Kanazawa University
- Li Chen
- Department of Medicine, Cedars-Sinai Medical Center
- Jin-Fen Xiao
- Cancer Science Institute of Singapore, National University of Singapore
- Chun-Quan Li
- School of Medical Informatics, Daqing Campus, Harbin Medical University
- Mo-Li Huang
- Cancer Science Institute of Singapore, National University of Singapore
- Ling-Wen Ding
- Cancer Science Institute of Singapore, National University of Singapore
- Qiao-Yang Sun
- Cancer Science Institute of Singapore, National University of Singapore
- Liang Xu
- Cancer Science Institute of Singapore, National University of Singapore
- Deepika Kanojia
- Cancer Science Institute of Singapore, National University of Singapore
- Maya Jeitany
- Cancer Science Institute of Singapore, National University of Singapore
- Jian-Wen Deng
- Department of Biochemistry and Molecular Biology, Medical College of Shantou University
- Lian-Di Liao
- Institute of Oncologic Pathology, Medical College of Shantou University
- Harmik J. Soukiasian
- Department of Surgery, Cedars-Sinai Medical Center
- Benjamin P. Berman
- Center for Bioinformatics and Functional Genomics, Cedars-Sinai Medical Center
- Jia-Jie Hao
- State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College
- Li-Yan Xu
- Institute of Oncologic Pathology, Medical College of Shantou University
- En-Min Li
- Department of Biochemistry and Molecular Biology, Medical College of Shantou University
- Ming-Rong Wang
- State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College
- Xin-Gang Bi
- Department of Urology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College
- De-Chen Lin
- Department of Medicine, Cedars-Sinai Medical Center
- H. Phillip Koeffler
- Cancer Science Institute of Singapore, National University of Singapore
- DOI
- https://doi.org/10.1038/s41467-018-06081-9
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 13
Abstract
Master regulator transcription factors TP63 and SOX2 have been reported to overlap in genomic occupancy in squamous cell carcinomas (SCCs). Here, the authors demonstrate that TP63 and SOX2 promote co-operatively long non-coding RNA CCAT1 expression through activating its super-enhancer, and CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR super-enhancers and enhances both the MEK/ERK1/2 and PI3K/AKT signaling pathways in SCC.