RT  - European Journal of Gynaecological Oncology
ID  - 10.22514/ejgo.2022.033
T1  - Knockdown of FAM83D inhibits endometrial cancer cell viability and induces autophagy via the PI3K/AKT/mTOR axis
A1  - Zhou Cai
A1  - Yan Mei
A1  - Xiaoye Jiang
A1  - Ruiqin Li
K1  - FAM83D; Endometrial cancer (EC); Apoptosis; Autophagy; PI3K/AKT/mTOR pathway
YR  - 2022
SP  - 64
AB  - <p>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 (<i>FAM83D</i>) is proved to have carcinogenic properties and act as a new oncogene.<i> FAM83D</i> is overexpressed in endometrial cancer, but the role of <i>FAM83D</i> in EC is still unclear. Here the role of <i>FAM83D</i> was investigated in EC progression. <i>FAM83D</i> depletion inhibited the proliferation of EC cells. The knockdown of <i>FAM83D</i> induced EC cell cycle arrest. Moreover, its depletion stimulated the apoptosis and autophagy of EC cells. We further found <i>FAM83D </i>depletion inhibited progression of EC via targeting phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) axis. We therefore thought <i>FAM83D</i> could serve as a EC target.</p><p><br></p>