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The Kaohsiung journal of medical sciences, 2021-04, Vol.37 (4), p.286-293
2021
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Autor(en) / Beteiligte
Titel
MiR‐146a functions as a potential tumor suppressor in retinoblastoma by negatively regulate neuro‐oncological ventral antigen‐1
Ist Teil von
  • The Kaohsiung journal of medical sciences, 2021-04, Vol.37 (4), p.286-293
Ort / Verlag
BP, Asia: Wiley Publishing Asia Pty Ltd
Erscheinungsjahr
2021
Quelle
Wiley Online Library Journals
Beschreibungen/Notizen
  • MicroRNAs (miRNAs) are dysregulated in many tumors and have been found to play crucial roles in cancer biology. Retinoblastoma is a rare tumor that develops rapidly from a malignant tumor of immature cells in the retina known as photoreceptor progenitors. Our study aimed to explore the role of miR‐146a in the pathology of retinoblastoma. Potential target gene of miR‐146a was predicted by Targetscan. Reverse transcription quantitative polymerase chain reaction (RT‐PCR) showed that miR‐146a was downregulated and ventral nerve tumor antigen 1 (Neuro ‐ oncological ventral antigen 1, NOVA1) was upregulated in retinoblastoma. Luciferase assay confirmed that miR‐146a directly target NOVA1. MiR‐146a knockdown and overexpression experiments were performed and found that miR‐146a could regulate the expression of NOVA1. The miR‐146a knockdown and overexpression experiments were conducted to investigate the biological function of miR‐146a. MiR‐146a was found inhibited the viability, proliferation and invasion of retinoblastoma cell by MTT, EdU, and transwell assays. Flow cytometry was performed for the apoptosis analysis and miR‐146a increased the apoptosis of retinoblastoma cell was found. Above phenomenon can be rescued by overexpression of NOVA1. In conclusion, these results suggest that miR‐146a acts as a tumor suppressor and can act as a potential therapeutic target for retinoblastoma in the future.
Sprache
Englisch
Identifikatoren
ISSN: 1607-551X
eISSN: 2410-8650
DOI: 10.1002/kjm2.12337
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_82fc78282500412fb55eb1bb88770d4e

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