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miRNA‐126 enhances viability, colony formation, and migration of keratinocytes HaCaT cells by regulating PI3 K/AKT signaling pathway
Author(s) -
Chang Lili,
Liang Jinning,
Xia Xiujuan,
Chen Xianjin
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11088
Subject(s) - hacat , wound healing , protein kinase b , viability assay , gene knockdown , keratinocyte , microrna , cell migration , microbiology and biotechnology , cell growth , pi3k/akt/mtor pathway , cancer research , signal transduction , biology , chemistry , cell , cell culture , immunology , gene , biochemistry , genetics
Wound healing is a basic biological process including proliferation and migration of keratinocyte. The effects of microRNAs on skin wound healing remain largely unexplored. This study aimed to investigate the role of microRNA‐126 (miR‐126) in human skin wound healing. Relative expression of miR‐126 after injury was evaluated by qRT‐PCR. Cell viability, colony formation, cycle distribution, migration, and the alternation of PI3 K/AKT pathway after miR‐126 knockdown or overexpression were detected, respectively. In addition, potential target gene of miR‐126 was also explored by luciferase assay. Results showed that miR‐126 was up‐regulated during skin wound healing. Moreover, overexpression of miR‐126 promoted cell proliferation and migration, whereas inhibition of miR‐126 led to the opposite effects. Additionally, we discovered that PLK2, which inhibited cell viability, colony formation and migration of keratinocyte, was a target gene of miR‐126. The expression of PLK2 was negatively correlated with the level of miR‐126 during wound healing. Finally, we demonstrated that overexpression of miR‐126 significantly increased the expression of p‐AKT, p‐ERK2, and PI3 K, indicating that overexpression of miR‐126 activated PI3 K/AKT signaling pathway. In conclusion, our results demonstrated that miR‐126 acted as a critical regulator for promoting proliferation and migration in keratinocyte during skin wound healing.