Please use this identifier to cite or link to this item: https://doi.org/10.3389/fcell.2021.586150
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dc.titlePATZ1 (MAZR) Co-occupies Genomic Sites With p53 and Inhibits Liver Cancer Cell Proliferation via Regulating p27
dc.contributor.authorNg, Zhen Long
dc.contributor.authorSiew, Jiamin
dc.contributor.authorLi, Jia
dc.contributor.authorJi, Guanxu
dc.contributor.authorHuang, Min
dc.contributor.authorLiao, Xiaohua
dc.contributor.authorYu, Sue
dc.contributor.authorChew, Yuanyuan
dc.contributor.authorPng, Chin Wen
dc.contributor.authorZhang, Yongliang
dc.contributor.authorWen, Shijun
dc.contributor.authorYang, Henry
dc.contributor.authorZhou, Yiting
dc.contributor.authorLong, Yun Chau
dc.contributor.authorJiang, Zhi Hong
dc.contributor.authorWu, Qiang
dc.date.accessioned2022-10-13T07:55:48Z
dc.date.available2022-10-13T07:55:48Z
dc.date.issued2021-02-01
dc.identifier.citationNg, 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. https://doi.org/10.3389/fcell.2021.586150
dc.identifier.issn2296-634X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/233245
dc.description.abstractLiver 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.
dc.publisherFrontiers Media S.A.
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2021
dc.subjectCDKN1B/p27
dc.subjectChIP-seq
dc.subjectliver cancer proliferation
dc.subjectp53
dc.subjectPATZ1
dc.typeArticle
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.contributor.departmentMICROBIOLOGY AND IMMUNOLOGY
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.3389/fcell.2021.586150
dc.description.sourcetitleFrontiers in Cell and Developmental Biology
dc.description.volume9
dc.description.page586150
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