Journal of cellular and molecular medicine, 2017-11, Vol.21 (11), p.3055-3065
2017
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- Autor(en) / Beteiligte
- Titel
- DLEU1 contributes to ovarian carcinoma tumourigenesis and development by interacting with miR‐490‐3p and altering CDK1 expression
- Ist Teil von
- Journal of cellular and molecular medicine, 2017-11, Vol.21 (11), p.3055-3065
- Ort / Verlag
- England: John Wiley and Sons Inc
- Erscheinungsjahr
- 2017
- Quelle
- Wiley-Blackwell Journals
- Beschreibungen/Notizen
- Recently, a large number of studies have focused on the important role of long non‐coding RNAs (lncRNAs) in metabolism and development and have found that abnormal lncRNA expression is associated with the pathogenesis and development of many diseases. The lncRNA DLEU1 is involved in many solid tumours and haematological malignancies. However, its role in epithelial ovarian carcinoma (EOC) and the associated molecular mechanisms has not been reported. In this study, quantitative reverse transcription–PCR (qRT–PCR) demonstrated higher lncRNADLEU1 expression in EOC tissues than in normal tissues. Plasmid transfection of DLEU1 to up‐regulate its expression in the ovarian cancer cell lines A2780 and OVCAR3 increased cell proliferation, migration, and invasion, while inhibited apoptosis. Nude mouse xenograft assay demonstrated that DLEU1 overexpression promoted tumour growth in vivo. QRT–PCR showed decreased miR‐490‐3p expression, while Western blotting demonstrated increased its target genes CDK1, cyclinD1 and SMARCD1, as well as matrix metalloproteinase‐2 (MMP2), Bcl‐xL and P70S6K protein expression, respectively. Short interfering RNA silencing of DLEU1 produced opposite results, where qRT–PCR showed increased miR‐490‐3p expression. The dual‐luciferase reporter assay revealed a direct interaction between DLEU1 and miR‐490‐3p. MiR‐490‐3p plays a tumour suppressor role in epithelial ovarian cancer by targeting CDK1 regulation and influencing SMARCD1 and cyclin D1 (CCND1) expressions. Therefore, we suggest that through interaction with miR‐490‐3p, DLEU1 may influence the expression of CDK1, CCND1 and SMARCD1 protein, subsequently promoting the development and progression of EOC.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1582-1838eISSN: 1582-4934DOI: 10.1111/jcmm.13217Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5661118
- Format
- –
- Schlagworte
- Animals, bcl-X Protein - genetics, bcl-X Protein - metabolism, Carcinogenesis - genetics, Carcinogenesis - metabolism, Carcinogenesis - pathology, CDC2 Protein Kinase - genetics, CDC2 Protein Kinase - metabolism, CDK1, Cell Line, Tumor, Cell Movement, Cell Proliferation, Chromosomal Proteins, Non-Histone, Cyclin D1 - genetics, Cyclin D1 - metabolism, development, DLEU1, epithelial ovarian carcinoma, Female, Gene Expression Regulation, Neoplastic, Humans, Matrix Metalloproteinase 2 - genetics, Matrix Metalloproteinase 2 - metabolism, Mice, Mice, Nude, MicroRNAs - genetics, MicroRNAs - metabolism, miR‐490‐3p, Neoplasm Transplantation, Original, Ovarian Neoplasms - genetics, Ovarian Neoplasms - metabolism, Ovarian Neoplasms - pathology, Ribosomal Protein S6 Kinases, 70-kDa - genetics, Ribosomal Protein S6 Kinases, 70-kDa - metabolism, RNA, Long Noncoding - antagonists & inhibitors, RNA, Long Noncoding - genetics, RNA, Long Noncoding - metabolism, RNA, Small Interfering - genetics, RNA, Small Interfering - metabolism, Signal Transduction, Transcription Factors - genetics, Transcription Factors - metabolism, Tumor Suppressor Proteins - antagonists & inhibitors, Tumor Suppressor Proteins - genetics, Tumor Suppressor Proteins - metabolism, tumourigenesis