ArticleJournal of molecular neuroscience : MN2018
Suppression of Disheveled-Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- MicroRNAs' Significance in Retinoblastoma Diagnosis and Treatment: The Little Heroes.Biochemical genetics · 2025Review
- The role of mitochondrial/metabolic axis in development of tamoxifen resistance in breast cancer.Human cell · 2023Review
- Metabolic/hypoxial axis predicts tamoxifen resistance in breast cancer.Scientific reports · 2022Article
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
- The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA.Frontiers in oncology · 2020Review
- Expression profiles and prognostic value of miRNAs in retinoblastoma.Journal of cancer research and clinical oncology · 2019Review
- MicroRNA-98 targets HMGA2 to inhibit the development of retinoblastoma through mediating Wnt/β-catenin pathway.Cancer biomarkers : section A of Disease markers · 2019Article
- Non-Coding RNAs in Retinoblastoma.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence shows that Disheveled-Axin domain containing 1 (DIXDC1) is dysregulated in various cancers. However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We found that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Moreover, overexpression of DIXDC1 markedly reversed the antitumor effect of miR-186. Overall, our results reveal that DIXDC1 functions as a potential oncogene in RB, and inhibiting DIXDC1 by miR-186 suppresses the proliferation and invasion of RB cell lines. Our study suggests that DIXDC1 and miR-186 may serve as novel therapeutic targets for the treatment of RB.
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