Abstract:
:MOF is a well-known histone acetyltransferase to catalyze acetylation of histone H4 lysine 16 (K16), and it is relevant to diverse biological processes, such as gene transcription, cell cycle, early embryonic development and tumorigenesis. Here, we identify MOF as an oncogene in most thyroid cancer. It is found that expression level of MOF was significantly upregulated in most thyroid cancer tissue samples and cell lines. MOF-deficient in both BHP-10-3 and TT2609 cell lines inhibited cell proliferation by blocking the cell cycle in G1 phase and enhanced cell apoptosis. Mechanistically, MOF bound the TNK2 promoter to activate TNK2 transcription. Furthermore, the expression level of TNK2 was decreased with the histone acetyltransferase inhibitor. Besides, MOF promoted proliferation of thyroid cancer cells through increased phosphorylation of AKT, thus activating the PI3K/AKT pathway. Ultimately, our findings indicated that MOF played an oncogene role in development and progression of thyroid cancer and may be a potential novel target for the treatment of thyroid cancer.
journal_name
Front Pharmacoljournal_title
Frontiers in pharmacologyauthors
Li D,Yang Y,Chen B,Guo X,Gao S,Wang M,Duan M,Li Xdoi
10.3389/fphar.2020.607605subject
Has Abstractpub_date
2020-12-08 00:00:00pages
607605issn
1663-9812pii
607605journal_volume
11pub_type
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