Upregulation of FAM83F by c-Myc promotes cervical cancer growth and aerobic glycolysis via Wnt/β-catenin signaling activation
Upregulation of FAM83F by c-Myc promotes cervical cancer growth and aerobic glycolysis via Wnt/β-catenin signaling activation
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DOI：
10.1038/s41419-023-06377-9
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
litian
中科院分区：
文献类型：
--
作者：
zhangchanglin;liulixiang;liweizhao;limengxiong;zhangxunzhi;zhangchi;yanghuan;xiejiayuan;panwei;guoxue;shepeng;zhongli;litian
Cervical cancer (CC) seriously affects women’s health. Therefore, elucidation of the exact mechanisms and identification of novel.therapeutic targets are urgently needed. In this study, we identified FAM83F, which was highly expressed in CC cells and tissues, as.a potential target. Our clinical data revealed that FAM83F protein expression was markedly elevated in CC tissues and was positively.correlated with poor prognosis. Moreover, we observed that FAM83F knockdown significantly inhibited cell proliferation, induced.apoptosis, and suppressed glycolysis in CC cells, while its overexpression displayed opposite effects. Mechanistically, FAM83F.regulated CC cell growth and glycolysis by the modulation of Wnt/β-catenin pathway. The enhancing effects of FAM83F.overexpression on CC cell proliferation and glycolysis could be impaired by the Wnt/β-catenin inhibitor XAV939. Moreover, we.found that c-Myc bound to the FAM83F promoter and activated the transcription of FAM83F. Notably, knockdown of FAM83F.impaired the enhancement of cell proliferation and glycolysis induced by ectopic c-Myc. Consistent with in vitro findings, results.from a xenograft mouse model confirmed the promoting role of FAM83F. In summary, our study demonstrated that FAM83F.promoted CC growth and glycolysis through regulating the Wnt/β-catenin pathway, suggesting that FAM83F may be a potential.molecular target for CC treatment.
