Knockdown of FAM83D inhibits endometrial cancer cell viability and induces autophagy via the PI3K/AKT/mTOR axis
1Department of Medical, Wuhan City College, 430083 Wuhan, Hubei, China
2Department of Obstetrics and Gynecology, Yulin First Hospital, 718000 Yulin, Shaanxi, China
DOI: 10.22514/ejgo.2022.033 Vol.43,Issue 4,August 2022 pp.64-71
Submitted: 25 May 2022 Accepted: 04 July 2022
Published: 15 August 2022
*Corresponding Author(s): Ruiqin Li E-mail: email@example.com
It is important to search new diagnostic and prognostic markers of endometrial cancer (EC) and uncover the possible mechanisms. Family with sequence similarity 83 member D (FAM83D) is proved to have carcinogenic properties and act as a new oncogene. FAM83D is overexpressed in endometrial cancer, but the role of FAM83D in EC is still unclear. Here the role of FAM83D was investigated in EC progression. FAM83D depletion inhibited the proliferation of EC cells. The knockdown of FAM83D induced EC cell cycle arrest. Moreover, its depletion stimulated the apoptosis and autophagy of EC cells. We further found FAM83D depletion inhibited progression of EC via targeting phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) axis. We therefore thought FAM83D could serve as a EC target.
FAM83D; Endometrial cancer (EC); Apoptosis; Autophagy; PI3K/AKT/mTOR pathway
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