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

  • Dose Response. 2020 Jun 3;18(2):1559325820929234. doi: 10.1177/1559325820929234.
Chen Zhang  1 ,  Xiongxiong Xie  1 ,  Yawen Yuan  1 ,  Yimeng Wang  1 ,  Meijuan Zhou  1 ,  Xiangzhi Li  1  2 ,  Peilin Zhen  3
Affiliations
  • 1. Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
  • 2. Department of Public Health, Medical College, Guangxi University of Science and Technology, Liuzhou, China.
  • 3. Jiangmen Central Hospital, Affiliated Jiangmen Hospital of Sun Yat-sen University, Jiangmen, China.
PMID: 32547335 DOI: 10.1177/1559325820929234
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.

Keywords
ARMC8; HaCaT cell; UVB; apoptosis; miR-664; proliferation.
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