The micro RNA hsa-miR-377-3p inhibits tumor growth in malignant melanoma
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Updated: Sep 24, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Jian Yuan1, Lei Jiang2, Chaotang Guo3
1TEDA Institute of Biological Sciences and Biotechnology, Nankai University Tianjin 300457 P. R. China yj1993@mail.nankai.edu.cn.
Background/Aims:
Most recently, micro RNAs (miRNAs/miRs) have been suggested to play a key role in various physiological and pathological processes by regulating the expression of specific genes. The influence of miR-377-3p on multitudinous cancer cells has been investigated; however, its function in melanoma remains undiscovered. Armadillo repeat-containing protein 8 (ARMC8), a target of miR-377-3p, plays essential roles in proliferation, differentiation and apoptosis. Our research aimed to detect the specific roles of miR-377-3p in melanoma.
Methods:
The MiRNA and mRNA expressions were evaluated by a real-time quantitative polymerase chain reaction in the A375 and HEMa-LP cell lines. We predicted the possible interactions between microRNA and mRNAs by bioinformatics database and constructed them with the Cytoscape software. The proliferation and migration activities were investigated using a cell counting kit-8 (CCK8) and wound-healing assay. Validation of the correlation between miR-377-3p and ARMC8 was implemented by the luciferase reporter assay and PCR.
Results:
The expression of miR-377-3p was found to be lower in malignant melanoma cells. The upregulation of miR-377-3p inhibited the melanoma cell proliferation, migration, and ARMC8 expression. miR-377-3p was identified to bind to the 3'UTR region of ARMC8 directly; this indicated that miR-377-3p suppressed melanoma cell growth partly mediated via the ARMC8 expression.
Conclusion:
These findings show that miR-377-3p negatively regulates tumor growth in malignant melanoma, which may thus provide a potential biological target for melanoma treatment and subsequently lead to the development of potential treatments.
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