Abstract:
:Histone acetyltransferase MOF is involved in active transcription regulation through histone H4K16 acetylation. MOF is downexpressed in a number of human tumors, but biological function of MOF in endometrial cancer has not been fully defined. The estrogen receptor α (ERα) is a transcription factor that regulates estrogen-stimulated cell proliferation in hormone-responsive tumors. However, ERα expression is decreased in grade III ECa samples and high expression of ERα is associated with long disease-free survival in ECa. The molecular mechanism for these observations is still unclear. Here we demonstrate knockdown of MOF promotes ECa cell growth and proliferation in vitro and in vivo. Clinical evidence indicates that expression MOF is decreased and positively correlated with that of ERα in ECa tissues. Furthermore, MOF physically interacts with ERα and modulates ERα stability in ECa cells. In addition, MOF modulates expression of a subset of endogenous genes regulated by ERα. Taken together, our results define MOF as a potential tumor suppressor in ECa participates in maintenance of ERα protein stability and regulation of ERα action.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Wu Y,Zeng K,Wang C,Wang S,Sun H,Liu W,Wang X,Niu J,Cong SY,Zhou X,Zhao Ydoi
10.1016/j.bbrc.2018.10.090subject
Has Abstractpub_date
2019-02-05 00:00:00pages
541-548issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(18)32246-0journal_volume
509pub_type
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