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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	endometrial cancer
ICD-0-3	NA
Methods	qPCR, Western blot, RIP etc.
Sample	endometrial carcinoma tissues, cell lines (Ishikawa, HEC-1B and KLE)
Expression Pattern	down-regulated
Function Description	In order to focus on the role and mechanism of lncRNA DLEU1 in endometrial carcinoma, we used qRT-PCR to detect the expression of lncRNA DLEU1 and found that lncRNA DLEU1 was highly expressed in endometrial carcinoma. Moreover, compared to Ishikawa and KLE, lncRNA DLEU1 was higher in HEC-1B. In addition, Up-regulation of lncRNA DLEU1 promoted cell viability, migration, invasion and reduced the proportion of apoptosis. Otherwise, Down-regulation of lncRNA DLEU1 produced opposite results. Xenograft nude mice model assay showed that lncRNA DLEU1 can promote tumorigenesis in vivo. RiP confirmed that lncRNA DLEU1 could bind to mTOR. The rescue experiments revealed that silence of mTOR after up-regulation of lncRNA DLEU1 resulted in decrease of cell viability, migration and invasion and increase of apoptosis. The expression changes of PI3K, AKT1, p70S6K, rpS6, GSK3B, STAT3 and Bcl-xl were consistent with lncRNA DLEU1 and mTOR in western blot. Thus, we suggest that lncRNA DLEU1 combines with mTOR and then increases the expression of PI3K/AKT/mTOR pathway to promote endometrial carcinoma tumorigenesis and progression.
Pubmed ID	29745433
Year	2018
Title	lncRNA DLEU1 contributes to tumourigenesis and development of endometrial carcinoma by targeting mTOR.

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