KAISO, a critical regulator of p53-mediated transcription of CDKN1A and apoptotic genes
Authors: Dong-In Koh
Jin Young Kim
Albert B Reynolds
Min-Kyeong Kim
Man-Wook Hur
Hoon Ryu
Bu-Nam Jeon
Youngsoo Kim
Lee Parry
Won-Il Choi
Dohyun Han
Alan R Clarke
Journal: Proceedings of the National Academy of Sciences of the United States of America (2014)
Discipline: Multidisciplinary
Keywords: KAISO; apoptosis; cell cycle arrest; p300; p53.
Affiliations: Brain Korea 21 Plus Project for Medical Sciences, Department of Biochemistry and Molecular Biology, Severance Biomedical Research Institute, Yonsei University School of Medicine, SeoDaeMoon-Ku, Seoul 120-752, Korea;, Department of Biomedical Sciences and Biomedical Engineering, Seoul National University College of Medicine, Seoul 110-799, Korea;, VA Boston Healthcare System and Department of Neurology, Boston University School of Medicine, Boston, MA 02130;, Mass Spectrometry Research Center, Korea Basic Science Institute, Ochang-eup, Cheongwon-gun, Chungbuk 363-883, Korea;, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3XQ, United Kingdom; and., Department of Cell Biology, Vanderbilt University, Nashville, TN 37232-2175., Brain Korea 21 Plus Project for Medical Sciences, Department of Biochemistry and Molecular Biology, Severance Biomedical Research Institute, Yonsei University School of Medicine, SeoDaeMoon-Ku, Seoul 120-752, Korea; .

Abstract:  An unresolved issue in genotoxic stress response is identification of induced regulatory proteins and how these activate tumor suppressor p53 to determine appropriate cell responses. Transcription factor KAISO was previously described to repress transcription following binding to methylated DNA. In this study, we show that KAISO is induced by DNA damage in p53-expressing cells and then interacts with the p53-p300 complex to increase acetylation of p53 K320 and K382 residues, although decreasing K381 acetylation. Moreover, the p53 with this particular acetylation pattern shows increased DNA binding and potently induces cell cycle arrest and apoptosis by activating transcription of CDKN1A (cyclin-dependent kinase inhibitor 1) and various apoptotic genes. Analogously, in Kaiso KO mouse embryonic fibroblast cells, p53-to-promoter binding and up-regulation of p21 and apoptosis gene expression is significantly compromised. KAISO may therefore be a critical regulator of p53-mediated cell cycle arrest and apoptosis in response to various genotoxic stresses in mammalian cells. 

Retracted: No

PubPeer comments:
 This review paper appears to be unexpectedly similar to a 2014 PhD thesis by Ding Jian at the National University of Singapore called  Screening and Evaluation of the Anticancer Potential of Scorpion Venoms and Snake Venom L-Amino Acid Oxidase in Gastric Cancer . That thesis can be found here: https: core.ac.uk download pdf 48809206.pdf Here is a marked-up version of the text by Zhang and Zhang 2016, with highlighted text showing similarities to the Ding Jian 2014 thesis. Generated in SimTexter : ![file] ![file] Figure 1 from this paper (right) also looks very similar to Figure 1.6 from the Ding Jiang thesis (left): ![file] , 
 Retracted [4 September 2020] . --------------------------------------------- Following the publication of this article, an interested reader drew to our attention that the flow of the text, and the wording of numerous passages of text within the article, bore striking and unexpected similarities to the wording employed in a PhD thesis by Ding Jian at the National University of Singapore in 2014 entitled u201cScreening and Evaluation of the Anticancer Potential of Scorpion Venoms and Snake Venom L-Amino Acid Oxidase in Gastric Canceru201d. After having conducted an internal investigation, the Editor of Oncology Letters has determined beyond all reasonable doubt that the review submitted to the Journal shared an unacceptable level of identity with the PhD thesis by Ding Jian. The authors were contacted about these apparent similarities between their review and the thesis, and they agree to this retraction. The Editor of Oncology Letters deeply regrets that this article was not intercepted by our own checks for plagiarism prior to the publication of the review, and sincerely apologizes to the author of the PhD thesis and the readership for the inconvenience caused. We also thank the reader for bringing this matter to our attention. ,