IL28RA inhibits human epidermal keratinocyte proliferation by inhibiting cell cycle progression

2019 ◽  
Vol 46 (1) ◽  
pp. 1189-1197
Author(s):  
Xueli Yin ◽  
Shengquan Zhang ◽  
Bao Li ◽  
Yaohua Zhang ◽  
Xuejun Zhang
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Keratinocyte Proliferation ◽  
Epidermal Keratinocyte ◽  
Human Epidermal Keratinocyte

scholarly journals Lysophosphatidic Acid Mediates Imiquimod-Induced Psoriasis-like Symptoms by Promoting Keratinocyte Proliferation through LPAR1/ROCK2/PI3K/AKT Signaling Pathway

2021 ◽  
Vol 22 (19) ◽  
pp. 10777
Author(s):  
Donghee Kim ◽  
Hyo-Jin Kim ◽  
Jin-Ok Baek ◽  
Joo-Young Roh ◽  
Hee-Sook Jun
Keyword(s):  
Cell Cycle ◽  
Lysophosphatidic Acid ◽  
Cell Cycle Progression ◽  
Akt Signaling ◽  
Inflammasome Activation ◽  
Hacat Cells ◽  
Cycle Progression ◽  
Keratinocyte Proliferation ◽  
P27kip1 Expression ◽  
Cyclin A2

Psoriasis is a chronic inflammatory skin disease. Recently, lysophosphatidic acid (LPA)/LPAR5 signaling has been reported to be involved in both NLRP3 inflammasome activation in macrophages and keratinocyte activation to produce inflammatory cytokines, contributing to psoriasis pathogenesis. However, the effect and molecular mechanisms of LPA/LPAR signaling in keratinocyte proliferation in psoriasis remain unclear. In this study, we investigated the effects of LPAR1/3 inhibition on imiquimod (IMQ)-induced psoriasis-like mice. Treatment with the LPAR1/3 antagonist, ki16425, alleviated skin symptoms in IMQ-induced psoriasis-like mouse models and decreased keratinocyte proliferation in the lesion. It also decreased LPA-induced cell proliferation and cell cycle progression via increased cyclin A2, cyclin D1, cyclin-dependent kinase (CDK)2, and CDK4 expression and decreased p27Kip1 expression in HaCaT cells. LPAR1 knockdown in HaCaT cells reduced LPA-induced proliferation, suppressed cyclin A2 and CDK2 expression, and restored p27Kip1 expression. LPA increased Rho-associated protein kinase 2 (ROCK2) expression and PI3K/AKT activation; moreover, the pharmacological inhibition of ROCK2 and PI3K/AKT signaling suppressed LPA-induced cell cycle progression. In conclusion, we demonstrated that LPAR1/3 antagonist alleviates IMQ-induced psoriasis-like symptoms in mice, and in particular, LPAR1 signaling is involved in cell cycle progression via ROCK2/PI3K/AKT pathways in keratinocytes.

scholarly journals A ubiquitin-like protein encoded by the “noncoding” RNA TINCR promotes keratinocyte proliferation and wound healing

PLoS Genetics ◽  
2021 ◽  
Vol 17 (8) ◽  
pp. e1009686
Author(s):  
Akihiro Nita ◽  
Akinobu Matsumoto ◽  
Ronghao Tang ◽  
Chisa Shiraishi ◽  
Kazuya Ichihara ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Noncoding Rna ◽  
Cell Cycle Progression ◽  
Keratinocyte Differentiation ◽  
Epidermal Keratinocytes ◽  
Skin Wound Healing ◽  
Human Epidermal Keratinocytes ◽  
Cycle Progression ◽  
Keratinocyte Proliferation

Although long noncoding RNAs (lncRNAs) are transcripts that do not encode proteins by definition, some lncRNAs actually contain small open reading frames that are translated. TINCR (terminal differentiation–induced ncRNA) has been recognized as a lncRNA that contributes to keratinocyte differentiation. However, we here show that TINCR encodes a ubiquitin-like protein that is well conserved among species and whose expression was confirmed by the generation of mice harboring a FLAG epitope tag sequence in the endogenous open reading frame as well as by targeted proteomics. Forced expression of this protein promoted cell cycle progression in normal human epidermal keratinocytes, and mice lacking this protein manifested a delay in skin wound healing associated with attenuated cell cycle progression in keratinocytes. We termed this protein TINCR-encoded ubiquitin-like protein (TUBL), and our results reveal a role for TINCR in the regulation of keratinocyte proliferation and skin regeneration that is dependent on TUBL.

1955-P: GLP-1R Activation Attenuates Prostate Cancer Growth via Inhibiting Cell Cycle Progression

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1955-P
Author(s):  
TORU SHIGEOKA ◽  
TAKASHI NOMIYAMA ◽  
TAKAKO KAWANAMI ◽  
YURIKO HAMAGUCHI ◽  
TOMOKO TANAKA ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cancer Growth ◽  
Cycle Progression
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