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

Overview

Journal Dose Response

Publisher Sage Publications

Date 2020 Jun 18

PMID 32547335

Citations 3

Authors

Chen Zhang

Xiongxiong Xie

Yawen Yuan

Yimeng Wang

Meijuan Zhou

Xiangzhi Li

Peilin Zhen

Affiliations

Soon will be listed here.

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.

Citing Articles

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

Liang X, Zhang C, Shen L, Ding L, Guo H Exp Ther Med. 2024; 27(6):262.

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Downregulation of SMAD4 protects HaCaT cells against UVB-induced damage and oxidative stress through the activation of EMT.

Li X, Wang Y, Wang X, Shen Y, Yuan Y, He Q Photochem Photobiol Sci. 2024; 23(6):1051-1065.

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