IncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR

IncRNA DLEU1 as a non-coding gene, involves in the occurrence and development of multiple tumors. However, there is no related report in endometrial carcinoma. In order to focus on the role and mechanism of IncRNA DLEU1 in endometrial carcinoma, we used qRT-PCR to detect the expression of IncRNA DLEU1 and found that IncRNA DLEU1 was highly expressed in endometrial carcinoma compared to normal endometrium. Moreover, compared to Ishikawa and KLE, IncRNA DLEU1 was higher in HEC-1B. In addition, up-regulation of IncRNA DLEU1 promoted cell viability, migration, invasion, and reduced the proportion of apoptosis. Otherwise, downregulation of IncRNA DLEU1 produced opposite results. Xenograft nude mice model assay showed that IncRNA DLEU1 can promote tumorigenesis in vivo. RiP confirmed that IncRNA DLEU1 could bind to mTOR. The rescue experiments revealed that silence of mTOR after up-regulation of IncRNA DLEU1 resulted in decrease of cell viability, migration, and invasion and increase of apoptosis. The expression changes of PI3K, AKT1, p70S6K, rpS6, GSK3 beta, STAT3, and Bcl-xl were consistent with IncRNA DLEU1 and mTOR in Western blot. Thus, we suggest that IncRNA DLEU1 combines with mTOR and then increases the expression of PI3K/AKT/mTOR pathway to promote endometrial carcinoma tumorigenesis and progression. The present discovery has probability to provide a biomarker and lay the foundation for targeted therapy of endometrial carcinoma.