Please use this identifier to cite or link to this item:
Title: PATZ1 (MAZR) Co-occupies Genomic Sites With p53 and Inhibits Liver Cancer Cell Proliferation via Regulating p27
Authors: Ng, Zhen Long
Siew, Jiamin
Li, Jia
Ji, Guanxu
Huang, Min
Liao, Xiaohua
Yu, Sue 
Chew, Yuanyuan
Png, Chin Wen 
Zhang, Yongliang 
Wen, Shijun
Yang, Henry 
Zhou, Yiting
Long, Yun Chau
Jiang, Zhi Hong
Wu, Qiang
Keywords: CDKN1B/p27
liver cancer proliferation
Issue Date: 1-Feb-2021
Publisher: Frontiers Media S.A.
Citation: Ng, Zhen Long, Siew, Jiamin, Li, Jia, Ji, Guanxu, Huang, Min, Liao, Xiaohua, Yu, Sue, Chew, Yuanyuan, Png, Chin Wen, Zhang, Yongliang, Wen, Shijun, Yang, Henry, Zhou, Yiting, Long, Yun Chau, Jiang, Zhi Hong, Wu, Qiang (2021-02-01). PATZ1 (MAZR) Co-occupies Genomic Sites With p53 and Inhibits Liver Cancer Cell Proliferation via Regulating p27. Frontiers in Cell and Developmental Biology 9 : 586150. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1/MAZR) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial largely due to lack of genome-wide studies. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma cells. Our PATZ1 ChIP-seq and gene expression microarray analyses revealed that PATZ1 is strongly related to cancer signatures and cellular proliferation. We further discovered that PATZ1 depletion led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Importantly, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, we found that PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its transcription. Notably, we demonstrated that PATZ1 is a p53 partner and p53 is essential for CDKN1B regulation. In conclusion, our study provides novel mechanistic insights into the inhibitory role of PATZ1 in liver cancer progression, thereby yielding a promising therapeutic intervention to alleviate tumor burden. © Copyright © 2021 Ng, Siew, Li, Ji, Huang, Liao, Yu, Chew, Png, Zhang, Wen, Yang, Zhou, Long, Jiang and Wu.
Source Title: Frontiers in Cell and Developmental Biology
ISSN: 2296-634X
DOI: 10.3389/fcell.2021.586150
Rights: Attribution 4.0 International
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_3389_fcell_2021_586150.pdf3.62 MBAdobe PDF



Google ScholarTM



This item is licensed under a Creative Commons License Creative Commons