Dataset Information

Long non-coding RNA UCA1 promotes retinoblastoma progression by modulating the miR-124/c-myc axis.

ABSTRACT: The long non-coding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1), belongs to cancer-related lncRNAs implicated in various carcinomas, including colorectal and gastric cancers. Nonetheless, the role and underlying mechanisms of UCA1 in retinoblastoma are still unclear. This study found that UCA1 expression in retinoblastoma tissues and cells was dramatically upregulated relative to that of healthy controls. Functionally, UCA1 knockdown could suppress retinoblastoma cells' proliferation, migration and invasion, and facilitate their apoptosis. Knockdown of UCA1 also retarded the growth of xenograft tumors in vivo. Mechanistically, UCA1 promoted c-myc expression through sponging miR-124. miR-124 inhibition or c-myc overexpression partially reversed the effects of UCA1 knockdown on retinoblastoma cells. Overall, lncRNA UCA1 may exert an oncogenic effect on retinoblastoma progression through the miR-124/c-myc axis, which might serve as a promising retinoblastoma treatment target.

SUBMITTER: Wang L

PROVIDER: S-EPMC8991135 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Long non-coding RNA UCA1 promotes retinoblastoma progression by modulating the miR-124/c-myc axis.

Wang Lan L Wu Mingxing M Zhou Xiyuan X

American journal of translational research 20220315 3

The long non-coding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1), belongs to cancer-related lncRNAs implicated in various carcinomas, including colorectal and gastric cancers. Nonetheless, the role and underlying mechanisms of UCA1 in retinoblastoma are still unclear. This study found that UCA1 expression in retinoblastoma tissues and cells was dramatically upregulated relative to that of healthy controls. Functionally, UCA1 knockdown could suppress retinoblastoma cells' proliferation, ...[more]

PMID: 35422898

Similar Datasets

Project description:BackgroundChordoma, an extremely rare malignant tumor, remains difficult to be cured because of its strong local invasiveness and high recurrence rate. Long non-coding RNAs (lncRNAs) have been demonstrated to play multiple roles in various cancers. The purpose of this study was to investigate the modulatory function of lncRNA MDFIC-7 in chordoma and to elucidate its underlying mechanisms.MethodsQuantitative real-time polymerase chain reaction was performed to detect the expression of lncRNA MDFIC-7 in tumor tissues and adjacent nontumorous tissues collected from 15 chordoma patients, as well as in chordoma cell lines. Gene silencing and overexpression experiments were carried out by RNA interference and lentiviral transduction. The effect of lncRNA MDFIC-7 on the proliferation of chordoma cells was evaluated by cell counting kit-8 assay, colony formation assay and xenograft tumor experiments. RNA immunoprecipitation and dual luciferase reporter assays were conducted to evaluate the binding between lncRNA MDFIC-7 and miRNA-525-5p and the interaction between miR-525-5p and the 3' untranslated region of ADP-ribosylation factor 6 (ARF6) mRNA. The glycolytic capacity and mitochondrial function of chordoma cells were measured by the Seahorse Bioscience XF96 Extracellular Flux Analyzer.ResultsThe expression of lncRNA MDFIC-7 was higher in chordoma tumor tissues than in adjacent non-tumor tissues. Downregulation of lncRNA MDFIC-7 reduced colony formation and cell proliferation in chordoma cells and decreased xenograft tumor growth in a nude mouse model. Moreover, lncRNA MDFIC-7 knockdown attenuated the Warburg effect in chordoma cells and xenograft tumors. LncRNA MDFIC-7 knockdown elevated miR-525-5p levels and decreased ARF6 expressions. Overexpression of ARF6 reversed the inhibitory effect of lncRNA MDFIC-7 knockdown on cell proliferation and the Warburg effect in chordoma cells and xenograft tumors. Mechanistically, lncRNA MDFIC-7, as a molecular sponge of miR-525-5p, negatively regulated miR-525-5p expression and promoted the gene expression of ARF6, a miR-525-5p target.ConclusionOur findings demonstrate that lncRNA MDFIC-7 acts as a molecular sponge to competitively bind to miR-525-5p and promote expression of ARF6. The lncRNA MDFIC-7/miR-525-5p/ARF6 axis regulates chordoma progression and the Warburg effect in chordoma, suggesting that lncRNA MDFIC-7 and miR-525-5p could be promising therapeutic targets for the treatment of chordoma.

Dataset Information

Long non-coding RNA UCA1 promotes retinoblastoma progression by modulating the miR-124/c-myc axis.

Publications

Long non-coding RNA UCA1 promotes retinoblastoma progression by modulating the miR-124/c-myc axis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets