<?xml version="1.0" encoding="UTF-8"?>
<records>
<record>
<language>eng</language>
<publisher>Science and Education Publishing</publisher>
<journalTitle>American Journal of Cancer Prevention</journalTitle>
<eissn>2328-7314</eissn>
<publicationDate>2022-06-05</publicationDate>
<volume>9</volume>
<issue>1</issue>
<startPage>4</startPage>
<endPage>9</endPage>
<doi>10.12691/ajcp-9-1-2</doi>
<publisherRecordId>AJCP2022912</publisherRecordId>
<documentType>article</documentType>
<title language="eng">The PCAF/WSTF/MOF Complex Regulates H3K9ac and H4K16ac in Breast Cancer Cells</title>
<authors>
<author>
<name>Ya-qi Wang</name>
<email>yaqiwang2008@163.com, jinghuazhang2014@163.com</email>
<affiliationId>1</affiliationId>
</author>
<author>
<name>Shunli-li Zhang</name>
<affiliationId>1</affiliationId>
</author>
<author>
<name>Jing-hua Zhang</name>
<email>yaqiwang2008@163.com, jinghuazhang2014@163.com</email>
<affiliationId>2</affiliationId>
</author>
<author>
<name>Shuqing Wang</name>
<affiliationId>3</affiliationId>
</author>
<author>
<name>Hong Wang</name>
<affiliationId>3</affiliationId>
</author>
<author>
<name>Yang Wang</name>
<affiliationId>3</affiliationId>
</author>
<author>
<name>Dan Li</name>
<affiliationId>4</affiliationId>
</author>

</authors>
<affiliationsList>
<affiliationName affiliationId="1">Department of Surgical Oncology, Tangshan People¡¯s Hospital, Tangshan, China</affiliationName>

<affiliationName affiliationId="2">Department of Surgical, Tangshan Women and Children¡¯s Hospital, Tangshan, China</affiliationName>
<affiliationName affiliationId="3">College of Life Science, North China University of Science and Technology, Tangshan, China</affiliationName>


<affiliationName affiliationId="4">Cancer Institute, Tangshan People¡¯s Hospital, Tangshan, China</affiliationName>
</affiliationsList>
<abstract language="eng">In order to study WSTF (Williams syndrome transcription factor) regulation mechanism involved in Ras signal related to breast cancer cells. Western blot was used to detect WSTF phosphorylation and histone modification levels. GST pull-down was conducted to testify the interaction between WSTF, PCAF and MOF. Acetyltransferase activity of PCAF and MOF was tested via HAT activity assay. ChIP and Real-time PCR were applied to confirm gene expression. In vivo tumor growth analysis was used to test tumor formation capability. Results revealed an interaction between WSTF, PCAF and MOF. WSTF phosphorylation increased following Ras activation with enhancement of the association between WSTF and PCAF while the association between WSTF and MOF was attenuated. The changes resulted in an increase of PCAF activity and decrease of MOF, and upregulation of H3K9ac and downregulation of H4K16ac followed by gene expression changes and enhancement of tumor formation. In conclusion, WSTF involved in regulation of PCAF and MOF, meanwhile, tumor formation was affected as a consequence of changes of H3K9ac, H4K16ac and tumor related gene expression.</abstract>
<fullTextUrl format="pdf">http://pubs.sciepub.com/ajcp/9/1/2/ajcp-9-1-2.pdf</fullTextUrl>
<keywords language="eng"><keyword>breast cancer</keyword>
<keyword>WSTF</keyword>
<keyword>MOF</keyword>
<keyword>PCAF</keyword>
</keywords>
</record>
</records>
