Nature Communications (Apr 2020)
Targeting codon 158 p53-mutant cancers via the induction of p53 acetylation
- Li Ren Kong,
- Richard Weijie Ong,
- Tuan Zea Tan,
- Nur Afiqah Binte Mohamed Salleh,
- Matan Thangavelu,
- Jane Vin Chan,
- Lie Yong Judice Koh,
- Giridharan Periyasamy,
- Jieying Amelia Lau,
- Thi Bich Uyen Le,
- Lingzhi Wang,
- Miyoung Lee,
- Srinivasaraghavan Kannan,
- Chandra S. Verma,
- Chwee Ming Lim,
- Wee Joo Chng,
- David P. Lane,
- Ashok Venkitaraman,
- Huynh The Hung,
- Chit Fang Cheok,
- Boon Cher Goh
Affiliations
- Li Ren Kong
- Cancer Science Institute of Singapore, National University of Singapore
- Richard Weijie Ong
- Laboratory of Molecular Endocrinology, National Cancer Centre Singapore
- Tuan Zea Tan
- Cancer Science Institute of Singapore, National University of Singapore
- Nur Afiqah Binte Mohamed Salleh
- Cancer Science Institute of Singapore, National University of Singapore
- Matan Thangavelu
- Genome Institute of Singapore, Agency for Science, Technology & Research (A*STAR)
- Jane Vin Chan
- Genome Institute of Singapore, Agency for Science, Technology & Research (A*STAR)
- Lie Yong Judice Koh
- Genome Institute of Singapore, Agency for Science, Technology & Research (A*STAR)
- Giridharan Periyasamy
- Genome Institute of Singapore, Agency for Science, Technology & Research (A*STAR)
- Jieying Amelia Lau
- Cancer Science Institute of Singapore, National University of Singapore
- Thi Bich Uyen Le
- Laboratory of Molecular Endocrinology, National Cancer Centre Singapore
- Lingzhi Wang
- Cancer Science Institute of Singapore, National University of Singapore
- Miyoung Lee
- Medical Research Council Cancer Unit, University of Cambridge
- Srinivasaraghavan Kannan
- Bioinformatics Institute, Agency for Science, Technology, and Research (A*STAR)
- Chandra S. Verma
- Bioinformatics Institute, Agency for Science, Technology, and Research (A*STAR)
- Chwee Ming Lim
- Division of Surgical Oncology (Head and Neck Surgery), National University Cancer Institute, Singapore (NCIS)
- Wee Joo Chng
- Cancer Science Institute of Singapore, National University of Singapore
- David P. Lane
- p53 Laboratory (p53Lab), Agency for Science, Technology, and Research (A*STAR)
- Ashok Venkitaraman
- Medical Research Council Cancer Unit, University of Cambridge
- Huynh The Hung
- Laboratory of Molecular Endocrinology, National Cancer Centre Singapore
- Chit Fang Cheok
- Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR)
- Boon Cher Goh
- Cancer Science Institute of Singapore, National University of Singapore
- DOI
- https://doi.org/10.1038/s41467-020-15608-y
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 17
Abstract
Codon 158 gain-of-function mutant p53 (158-mutp53) promotes tumourigenesis in lung cancer. Here, the authors show that 158-mutp53 render cancers sensitive to cisplatin and p53 acetylation agents through a mechanism where acetylated mutant p53 upregulates TRAIP and inhibits NF-ĸB signaling.
