PMID- 34518485 OWN - NLM STAT- MEDLINE DCOM- 20221019 LR - 20221019 IS - 1423-0399 (Electronic) IS - 0042-1138 (Linking) VI - 106 IP - 10 DP - 2022 TI - Silencing of lncRNA MEG8 Represses the Viability, Migration, and Invasion of Wilms' Tumor Cells through Mediating miR-23a-3p/CRK Axis. PG - 1075-1087 LID - 10.1159/000518502 [doi] AB - PURPOSE: Compelling evidence has unveiled the importance of long noncoding RNAs (lncRNAs) in malignant behavior of Wilms' tumor (WT). Hereon, we intend to assess the function and associated molecular mechanism of lncRNA maternally expressed gene 8 (MEG8) in WT cells. METHODS: Expression levels of MEG8, miR-23a-3p, and CT10 regulator of kinase (CRK) were determined by quantitative real-time polymerase chain reaction. Cell viability was assessed by MTT assay. Besides, wound healing assay and transwell assay were applied to examine abilities of cell migration and invasion, respectively. Dual-luciferase reporter assay was employed to test the interplay among MEG8, miR-23a-3p, and CRK. Western blot was used to detect relative protein expression of CRK. RESULTS: MEG8 and CRK expression was elevated, while miR-23a-3p expression was decreased in WT tissues and cells. The histologic type, lymphatic metastasis, and National Wilms Tumor Study (NWTS) stage were associated with the expression of MEG8, miR-23a-3p, and CRK in WT patients. MEG8 knockdown or miR-23a-3p overexpression restrained WT cells in cell viability, migration, and invasiveness in vitro. As to mechanism exploration, MEG8 could directly bind to miR-23a-3p and then miR-23a-3p targeted CRK. MEG8 was inversely correlated with miR-23a-3p and positively correlated with CRK in WT tissues. Meantime, miR-23a-3p was inversely correlated with CRK in WT tissues. Additionally, MEG8 knockdown-mediated suppressive impacts on cell viability, migration, and invasiveness were reversed by overexpression of CRK or repression of miR-23a-3p in WT cells. CONCLUSIONS: The cell viability, migration, and invasiveness of WT cells were repressed by MEG8 knockdown via targeting the miR-23a-3p/CRK axis. CI - (c) 2021 S. Karger AG, Basel. FAU - Shen, Jing AU - Shen J AD - National Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou City, China, victor11272020@163.com. FAU - Shu, Qiang AU - Shu Q AD - National Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou City, China. LA - eng PT - Journal Article DEP - 20210908 PL - Switzerland TA - Urol Int JT - Urologia internationalis JID - 0417373 RN - 0 (CRK protein, human) RN - 0 (MIRN23a microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Proto-Oncogene Proteins c-crk) RN - 0 (RNA, Long Noncoding) SB - IM MH - Cell Line, Tumor MH - Cell Movement MH - Cell Proliferation/genetics MH - Gene Expression Regulation, Neoplastic MH - Humans MH - *Kidney Neoplasms/genetics/metabolism MH - *MicroRNAs/genetics/metabolism MH - Proto-Oncogene Proteins c-crk/genetics/metabolism MH - *RNA, Long Noncoding/genetics/metabolism MH - *Wilms Tumor/genetics OTO - NOTNLM OT - CT10 regulator of kinase OT - Long noncoding RNA OT - Maternally expressed gene 8 OT - Wilms' tumor OT - miR-23a-3p EDAT- 2021/09/15 06:00 MHDA- 2022/10/20 06:00 CRDT- 2021/09/14 05:58 PHST- 2021/01/11 00:00 [received] PHST- 2021/07/14 00:00 [accepted] PHST- 2021/09/15 06:00 [pubmed] PHST- 2022/10/20 06:00 [medline] PHST- 2021/09/14 05:58 [entrez] AID - 000518502 [pii] AID - 10.1159/000518502 [doi] PST - ppublish SO - Urol Int. 2022;106(10):1075-1087. doi: 10.1159/000518502. Epub 2021 Sep 8.