Dysregulated function of normal human epidermal keratinocytes in the absence of filaggrin

Dang,Ningning; Ma,Xiaoli; Meng,Xianguang; An,Liguo; Pang,Shuguang

doi:10.3892/mmr.2016.5539

Dysregulated function of normal human epidermal keratinocytes in the absence of filaggrin

Authors:
- Ningning Dang
- Xiaoli Ma
- Xianguang Meng
- Liguo An
- Shuguang Pang
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Affiliations: Department of Dermatology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China, Central Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China, College of Life Science, Shandong Normal University, Jinan, Shandong 250014, P.R. China, Department of Endocrinology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, P.R. China
Published online on: July 22, 2016 https://doi.org/10.3892/mmr.2016.5539
Pages: 2566-2572
Copyright: © Dang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the impact of filaggrin knockdown on the function of normal human epidermal keratinocytes (NHEKs). Filaggrin expression levels in NHEKs were knocked down by lentivirus (LV) encoding small hairpin RNA (shRNA), with control cells infected with nonsense shRNA or not infected. Cell migration and invasion were assayed using Transwell inserts, cell adhesion and proliferation by the Cell Counting kit‑8 assay, and apoptosis and cell cycle progression by flow cytometry. shRNA efficiently suppressed expression of filaggrin protein. The LV group had significantly decreased cell migration, adhesion and proliferation, and increased apoptosis compared with the control groups (P=0.027). In addition, the proportion of cells in G1 and G2 phases were significantly increased in the LV group compared with control groups (P=0.018). The results of the present study demonstrate that filaggrin knockdown inhibits NHEK migration, adhesion and proliferation, promotes apoptosis and disturbs cell cycle progression.

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