Abstract
MicroRNAs (miRNAs/miRs) serve important roles in regulating gene expression by directly binding to the 3'‑untranslated regions of target genes. Multiple miRNAs are dysregulated in retinoblastoma (RB) and their dysregulation is closely related to RB malignancy. Therefore, exploring the detailed roles of miRNAs in RB is valuable to facilitate the development of effective therapeutic targets for patients with this disease. miRNA‑874‑3p (miR‑874) has been recently reported to be downregulated in several types of human cancer and serves an essential role in cancer progression. However, the expression pattern and detailed roles of miR‑874 in RB, aswellas the underlying molecular mechanisms in RB, have not been clearly elucidated. Therefore, this study detected miR‑874 expression in RB tissues and cell lines. The biological roles of miR‑874 in RB were determined and the underlying mechanisms of its actions in RB cells were also examined. This study revealed that miR‑874 expression was aberrantly underexpressed in RB tissues and cell lines. However, returning miR‑874 expression restricted the proliferative and invasive abilities of RB cells. In terms of the underlying mechanism, metadherin (MTDH) was validated as a direct target gene of miR‑874 in RB cells. MTDH inhibition could imitate the inhibitory roles of miR‑874 overexpression in RB cells. Furthermore, forced MTDH expression partially reversed the suppressive effects of miR‑874 on RB cells. In conclusion, this study revealed that miR‑874 may inhibit RB progression by directly targeting MTDH. Restoration of miR‑874 expression may be a novel strategy for preventing the rapid growth and metastasis of RB cells.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.