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LncRNA RP6‐65G23.1 accelerates proliferation and inhibits apoptosis via p‐ERK1/2/p‐AKT signaling pathway on keratinocytes
Author(s) -
Duan Qiqi,
Wang Guorong,
Wang Min,
Chen Caifeng,
Zhang Mengdi,
Liu Meng,
Shao Yongping,
Zheng Yan
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29685
Subject(s) - hacat , protein kinase b , downregulation and upregulation , gene knockdown , apoptosis , microbiology and biotechnology , signal transduction , cancer research , biology , cell growth , chemistry , cell culture , biochemistry , gene , genetics
Long non‐coding RNAs (LncRNAs) play essential roles in the development of various diseases including hepatic carcinoma, melanoma, and psoriasis. Meanwhile, lncRNA‐RP6‐65G23.1 was upregulated in psoriasis. However, it is still unclear whether lncRNA‐RP6‐65G23.1 expression is upregulated and contributes to keratinocytes proliferation and apoptosis, and which mechanisms are responsible for these processes. The aims of this study are to address these issues. RP6‐65G23.1 was significantly upregulated in M5‐stimulated keratinocytes and stimulated the proliferation and inhibited the apoptosis of HaCaT cells. Knockdown of RP6‐65G23.1 resulted in defects of growth and increased rates of apoptosis in HaCaT cells, while overexpression of RP6‐65G23.1 manifested the opposite effects. Consistently, the expression of antiapoptotic proteins Bcl‐xl and Bcl2 were decreased in RP6‐65G23.1‐knockdown cells but elevated in RP6‐65G23.1 overexpression cells. In addition, RP6‐65G23.1 depletion blunted the activity of extracellular regulated kinase 1/2 (ERK1/2) and AKT signaling pathways and induced G 1 /S‐growth arrest. By contrast, overexpression of RP6‐65G23.1 activates the ERK1/2 and AKT signaling pathways and inhibits the expression of p21 and p27 in an AKT‐dependent manner leading to promote the G1/S progression. Our results suggested that lncRNA‐RP6‐65G23.1 would contribute to the pathogenesis of psoriasis by regulating the proliferation and apoptosis of keratinocytes via the p‐ERK1/2 and p‐AKT pathways.