PMID- 31702026 OWN - NLM STAT- MEDLINE DCOM- 20200331 LR - 20200331 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 20 IP - 5 DP - 2019 Nov TI - Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway. PG - 4551-4557 LID - 10.3892/mmr.2019.10705 [doi] AB - Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the tumorigenesis and progression of various types of cancer. The lncRNA deleted in lymphocytic leukemia 1 (DLEU1) has been reported to be dysregulated in cancer cells and thus associated with tumor development; however, the role of DLEU1 in renal cell carcinoma (RCC) remains unclear. In the present study, DLEU1 was knocked down using small interfering RNA in the RCC cell lines KETR3 and 786‑O to determine the role of DLEU1. Cell Counting Kit‑8, colony formation, Transwell and flow cytometry assays were performed to assess the effects of DLEU1 on cell proliferation, migration, invasion and apoptosis in KETR3 and 786‑O cells. The protein expression levels of factors associated with apoptosis and epithelial‑mesenchymal transition (EMT) were examined by western blot. The results demonstrated that silencing DLEU1 decreased the growth capacity, migration and invasion of KETR3 and 786‑O cells. Additionally, loss of DLEU1 was observed to stimulate the mitochondrial pathway of cell apoptosis via regulation of the expression of Bcl‑2/Bax, cleaved caspase‑3 and cleaved caspase‑9 in KETR3 and 786‑O cells. Furthermore, DLEU1 knockdown significantly inhibited the protein kinase B (Akt) pathway by downregulating the expression of phosphorylated‑Akt, cyclin D1 and P70S6 kinase. In addition, depletion of DLEU1 was observed to impair the process of EMT in RCC cells via the upregulation of E‑cadherin, and downregulation of N‑cadherin and vimentin. Collectively, these results indicated a pro‑oncogenic role of DLEU1 in the progression and development of RCC via modulation of the Akt pathway and EMT phenotype. FAU - Yue, Genquan AU - Yue G AD - Department of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Chen, Caixia AU - Chen C AD - Clinical Medical Research Center, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Bai, Ligang AU - Bai L AD - Department of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Wang, Guoqiang AU - Wang G AD - Department of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Huang, Yong AU - Huang Y AD - Department of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Wang, Yunbin AU - Wang Y AD - Department of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Cui, Hongwei AU - Cui H AD - Clinical Medical Research Center, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China. FAU - Xiao, Yunfeng AU - Xiao Y AD - The Center for New Drug Safety Evaluation and Research of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010110, P.R. China. LA - eng PT - Journal Article DEP - 20190925 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (RNA, Long Noncoding) RN - 0 (RNA, Neoplasm) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) SB - IM MH - Carcinoma, Renal Cell/genetics/*metabolism/pathology MH - Cell Line, Tumor MH - *Down-Regulation MH - *Gene Expression Regulation, Enzymologic MH - *Gene Expression Regulation, Neoplastic MH - Gene Knockdown Techniques MH - Humans MH - Kidney Neoplasms/genetics/*metabolism/pathology MH - Proto-Oncogene Proteins c-akt/*biosynthesis/genetics MH - RNA, Long Noncoding/*biosynthesis/genetics MH - RNA, Neoplasm/*biosynthesis/genetics MH - *Signal Transduction PMC - PMC6797951 EDAT- 2019/11/09 06:00 MHDA- 2020/04/01 06:00 PMCR- 2019/09/25 CRDT- 2019/11/09 06:00 PHST- 2018/10/18 00:00 [received] PHST- 2019/04/09 00:00 [accepted] PHST- 2019/11/09 06:00 [pubmed] PHST- 2020/04/01 06:00 [medline] PHST- 2019/11/09 06:00 [entrez] PHST- 2019/09/25 00:00 [pmc-release] AID - mmr-20-05-4551 [pii] AID - 10.3892/mmr.2019.10705 [doi] PST - ppublish SO - Mol Med Rep. 2019 Nov;20(5):4551-4557. doi: 10.3892/mmr.2019.10705. Epub 2019 Sep 25.