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Article

The PCAF/WSTF/MOF Complex Regulates H3K9ac and H4K16ac in Breast Cancer Cells

1Department of Surgical Oncology, Tangshan People’s Hospital, Tangshan, China

2Department of Surgical, Tangshan Women and Children’s Hospital, Tangshan, China

3College of Life Science, North China University of Science and Technology, Tangshan, China

4Cancer Institute, Tangshan People’s Hospital, Tangshan, China


American Journal of Cancer Prevention. 2022, Vol. 9 No. 1, 4-9
DOI: 10.12691/ajcp-9-1-2
Copyright © 2022 Science and Education Publishing

Cite this paper:
Ya-qi Wang, Shunli-li Zhang, Jing-hua Zhang, Shuqing Wang, Hong Wang, Yang Wang, Dan Li. The PCAF/WSTF/MOF Complex Regulates H3K9ac and H4K16ac in Breast Cancer Cells. American Journal of Cancer Prevention. 2022; 9(1):4-9. doi: 10.12691/ajcp-9-1-2.

Correspondence to: Jing-hua  Zhang, Department of Surgical, Tangshan Women and Children’s Hospital, Tangshan, China. Email: yaqiwang2008@163.com, jinghuazhang2014@163.com

Abstract

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.

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