MiR-664 Protects Against UVB Radiation-Induced HaCaT Cell Damage via Downregulating ARMC8

Abstract

Background: MiR-664 has been demonstrated to play an important role in dermal diseases. However, the functions of miR-664 in ultraviolet B (UVB) radiation-induced keratinocytes damage remain to be elucidated. Objective: The present study aimed to investigate the molecular mechanisms under the UVB-induced keratinocytes damage and provide translational insights for future therapeutics and UVB protection. Methods: HaCaT cells were transfected with miR-664, either alone or combined with UVB irradiation. Levels of messenger RNA and protein were tested by quantitative real-time polymerase chain reaction and Western blot analyses. Cell proliferation, percentage of apoptotic cells, and expression levels of apoptosis-related factors were measured by Cell Counting Kit-8 assay, flow cytometry assay, and Western blot analysis, respectively. Results: We found that a significant increase in miR-664 was observed in UVB-induced HaCaT cells. Overexpressed miR-664 promoted cell vitalities and suppressed apoptosis of UVB-induced HaCaT cells. Additionally, the loss/gain of armadillo-repeat-containing protein 8 (ARMC8) rescued/blocked the effects of miR-664 on the proliferation of UVB-induced HaCaT cells. Conclusions: Our data demonstrate that miR-664 functions as a protective regulator in UVB-induced HaCaT cells via regulating ARMC8.

Structural and Functional Insights into GID/CTLH E3 Ligase Complexes

“…On the other hand, RanBP9 has been shown to be pro-apoptotic in a variety of cell lines via activation of the intrinsic pathway, as well as through other means, such as regulation of the MAPK pathway, aggresome formation, the activation of cofilin, and interactions with p73 and TSSC3 [ 132 , 142 , 143 , 145 , 146 , 147 ]. In keratinocytes, ARMC8 expression had a subtle positive effect on apoptosis induction in response to ultraviolet B radiation [ 148 ]. Meanwhile, WDR26 expression inhibited oxidative-stress-induced cell death in SH-SY5Y cells and cardiomyocytes [ 149 , 150 ].…”

Role of non‑coding RNAs in UV‑induced radiation effects (Review)

“…miR-27a directly reduced the expression and luciferase activity of target genes such as transactive response DNA-binding protein and apoptotic protease activating factor-1. A significant increase in miR-664 expression was observed in UVB-irradiated HaCaT cells, and overexpression of miR-664 promoted cell viability and inhibited UVB-induced apoptosis ( 51 ). Furthermore, the loss or gain of armadillo-repeat-containing protein 8 can rescue/block the effect of miR-664 on UVB-induced HaCaT cell proliferation.…”