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MiR-664 Protects Against UVB Radiation-Induced HaCaT Cell Damage via Downregulating ARMC8
Chen Zhang1, Xiongxiong Xie1, Yawen Yuan1
1Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
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.
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