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miR-498 promotes cell proliferation and inhibits cell apoptosis in retinoblastoma by directly targeting CCPG1

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Abstract

Purpose

Retinoblastoma (Rb) is the most common intraocular tumor in children. MicroRNAs (miRNAs) play a crucial role in gene regulation and cell growth/apoptosis/differentiation. The current study aimed to investigate the role of miR-498 in Rb.

Methods

Quantitative real-time polymerase chain reaction (QRT-PCR) was used to test mRNA level of miR-498. http://www.targetscan.org and http://www.microrna.org were applied to predict target of miR-498. Dual-luciferase reporter assay was applied to investigate if miR-498 targeted cell cycle progression 1 (CCPG1). Western blot (WB) was carried out to assess CCPG1 protein levels. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to evaluate cell proliferation. Annexin-V Fluorescein (FITC) was adopted to explore cell apoptosis.

Results

In Y79 cells, miR-498 was higher than in normal ARPE-19 cells. MiR-498 could recognize CCPG1-3′ untranslated region (UTR). CCPG1 protein level was remarkably decreased when overexpressed miR-498, nevertheless, significantly increased when inhibiting miR-498. Y79 cells that were transfected with miR-498 mimics manifested notable cell apoptosis down-regulation and cell proliferation promotion; whereas, those transfected with miR-498 inhibitor displayed significant cell apoptosis up-regulation and cell proliferation inhibition compared with control group.

Conclusion

Taken together, miR-498 promotes cell proliferation and inhibits cell apoptosis in Rb by directly targeting CCPG1.

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Acknowledgements

We thank Chao Lu from Department of Pediatrics, The First Affiliated Hospital, Nanjing Medical University, Nanjing, China, for his kind help in the current study.

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Correspondence to Qing-Huai Liu.

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Yang, L., Wei, N., Wang, L. et al. miR-498 promotes cell proliferation and inhibits cell apoptosis in retinoblastoma by directly targeting CCPG1. Childs Nerv Syst 34, 417–422 (2018). https://doi.org/10.1007/s00381-017-3622-8

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  • DOI: https://doi.org/10.1007/s00381-017-3622-8

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