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首页> 外文期刊>Biochemical and Biophysical Research Communications >miR-203a controls keratinocyte proliferation and differentiation via targeting the stemness-associated factor ΔNp63 and establishing a regulatory circuit with SNAI2
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miR-203a controls keratinocyte proliferation and differentiation via targeting the stemness-associated factor ΔNp63 and establishing a regulatory circuit with SNAI2

机译：miR-203a通过靶向茎颈相关因子Δnp63来控制角质形成细胞增殖和分化，并用snai2建立调节电路

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摘要

Abstract Keratinocyte differentiation plays a pivotal role in the function of epidermal barrier and can be triggered by extracellular calcium in?vitro and in?vivo , but the precise mechanism still need to be further investigated. On the other hand, it is known that microRNAs control multiple biological events including cellular proliferation and differentiation. The present study demonstrated that miR-203a expression was upregulated in calcium-induced HaCaT Cells in a dose-dependent manner, whereas the stemness-associated factors SNAI2 and ΔNp63 were downregulated. Furthermore, SNAI2 and ΔNp63 were identified as the targets of miR-203a by computational prediction and luciferase reporter assays. The protein levels of SNAI2 and ΔNp63 were suppressed by ectopic expression of miR-203a. Functionally, silencing of miR-203a or overexpression of SNAI2 and ΔNp63 attenuated cell cycle arrest induced by calcium without any changes in cellular apoptosis. Additionally, ectopic expression of SNAI2 inhibited miR-203a in calcium-induced HaCaT cells, by binding to the promoter region of miR-203a. In conclusion, our findings demonstrate that miR-203a plays an essential role in keratinocyte proliferation and differentiation caused by extracellular calcium by targeting the SNAI2 and ΔNp63 genes. Furthermore, SNAI2 was found to suppress the transcription of miR-203a. Our data highlights a coherent cross-talk between two transcription factors (SNAI2 and ΔNp63) and miR-203a in keratinocyte differentiation and epidermal development. Highlights ? miR-203a modulates keratinocyte proliferation and differentiation without any effect on apoptosis. ? The stemness-associated factors potentially targeted by miR-203a were screened and SNAI2 and ΔNp63 were confirmed. ? An auto-regulatory loop between miR-203a and SNAI2 plays a critical role in keratinocyte differentiation.
机译：摘要角质形成细胞分化在表皮屏障的功能中起着枢轴作用，并且可以通过细胞外钙在体外和体内引发，但仍需要进一步研究精确的机制。另一方面，已知微大RNA控制包括细胞增殖和分化的多种生物事件。本研究证明，MIR-203A表达以剂量依赖性方式在钙诱导的HACAT细胞中升高，而茎相关因子SNAI2和ΔNP63被下调。此外，通过计算预测和荧光素酶报告分析鉴定为MIR-203A的靶标。通过miR-203a的异位表达抑制Snai2和Δnp63的蛋白质水平。在功能上，MiR-203a的沉默或inai2和Δnp63的过表达衰减由钙引起的细胞周期停滞，而不会发生细胞凋亡的任何变化。另外，通过与miR-203a的启动子区结合，通过结合钙诱导的HaCAT细胞中Snai2的异位表达抑制miR-203a。总之，我们的研究结果表明MIR-203A通过靶向SNAI2和ΔNP63基因，在胰蛋白酶细胞增殖和分化中起重要作用。此外，发现Snai2抑制miR-203a的转录。我们的数据突出了三种转录因子（Snai2和Δnp63）和角质形成细胞分化和表皮发育的MiR-203a之间的相干串扰。强调 ？ miR-203a调节角质形成细胞增殖和分化，而不是对细胞凋亡的任何影响。还筛选miR-203a可能靶向的茎相关因子，并确认SNAI2和Δnp63。还miR-203a和snai2之间的自动调节环路在角质形成细胞分化中起着关键作用。

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  • 作者

    Xu Ma; Ling Li; Tao Jia; Mingwei Chen; Guofeng Liu; Chunyang Li; Ning Li; Daping Yang;

  • 作者单位

    Department of Plastic Surgery The Second Affiliated Hospital of Harbin Medical University;

    Department of Cardiology The Second Affiliated Hospital of Harbin Medical University;

    Department of Hand and Microsurgery The Second Affiliated Hospital of Harbin Medical University;

    Department of Anatomy Harbin Medical University;

    Department of Plastic Surgery The Second Affiliated Hospital of Harbin Medical University;

    Department of Plastic Surgery The Second Affiliated Hospital of Harbin Medical University;

    Department of Plastic Surgery The Second Affiliated Hospital of Harbin Medical University;

    Department of Plastic Surgery The Second Affiliated Hospital of Harbin Medical University;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    Epidermal differentiation; Keratinocyte; miR-203a; SNAI2; ΔNp63;

    机译：表皮分化;角质形成细胞;miR-203a;snai2;Δnp63;

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