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LINC00937 通过靶向 miR-28-5p/MC1R 轴抑制瘢痕疙瘩成纤维细胞增殖和细胞外基质沉积。

LINC00937 suppresses keloid fibroblast proliferation and extracellular matrix deposition by targeting the miR-28-5p/MC1R axis.

机构信息

Department of Dermatology, Renmin Hospital of Wuhan University, Wuhan, China.

Department of Dermatology, Huangshi Central Hospital of Edong Healthcare Group, Hubei Polytechnic University, Huangshi, Hubei, China.

出版信息

Histol Histopathol. 2021 Sep;36(9):995-1005. doi: 10.14670/HH-18-372. Epub 2021 Aug 23.

DOI:10.14670/HH-18-372
PMID:34486677
Abstract

Long noncoding RNAs (lncRNAs) are the most recently discovered class of noncoding RNAs. LncRNAs play a crucial role in multiple disorders. However, the role and mechanism of action of lncRNAs in keloids remain unclear. Here, qRT-PCR and western blotting assays were performed to determine the expression of genes and proteins, respectively. MTT assays were carried out to measure the proliferation of keloid fibroblasts. In addition, a luciferase activity assay was conducted to investigate the relationships between LINC00937 and miR-28-5p and between miR-28-5p and MC1R. The results showed that LINC00937 and MC1R were decreased, whereas miR-28-5p was increased in keloid tissues. LINC00937 overexpression in keloid fibroblasts could repress the extracellular matrix (ECM) deposition and cell proliferation and promote MC1R expression. Moreover, high expression of miR-28-5p and low expression of LINC00937 were detected in keloid fibroblasts. We further showed that LINC00937 promoted MC1R expression by sponging miR-28-5p. Finally, our data indicated that LINC00937 inhibited the ECM deposition and proliferation of keloid fibroblasts by inhibiting miR-28-5p and facilitating MC1R expression. Overall, LINC00937 suppressed the ECM deposition and proliferation of keloid fibroblasts by acting as an miR-28-5p sponge and promoting MC1R expression. Our data suggested that LINC00937 is a potential target for keloid treatment.

摘要

长链非编码 RNA(lncRNAs)是最近发现的一类非编码 RNA。lncRNAs 在多种疾病中发挥着关键作用。然而,lncRNAs 在瘢痕疙瘩中的作用和作用机制尚不清楚。在这里,分别进行了 qRT-PCR 和 Western blot 测定以确定基因和蛋白质的表达。进行了 MTT 测定以测量瘢痕疙瘩成纤维细胞的增殖。此外,进行了荧光素酶活性测定以研究 LINC00937 与 miR-28-5p 之间以及 miR-28-5p 与 MC1R 之间的关系。结果表明,LINC00937 和 MC1R 减少,而 miR-28-5p 在瘢痕疙瘩组织中增加。LINC00937 在瘢痕疙瘩成纤维细胞中的过表达可抑制细胞外基质(ECM)沉积和细胞增殖,并促进 MC1R 表达。此外,在瘢痕疙瘩成纤维细胞中检测到 miR-28-5p 高表达和 LINC00937 低表达。我们进一步表明,LINC00937 通过海绵吸附 miR-28-5p 促进 MC1R 表达。最后,我们的数据表明,LINC00937 通过抑制 miR-28-5p 并促进 MC1R 表达来抑制 ECM 沉积和瘢痕疙瘩成纤维细胞的增殖。总体而言,LINC00937 通过充当 miR-28-5p 海绵并促进 MC1R 表达来抑制瘢痕疙瘩成纤维细胞的 ECM 沉积和增殖。我们的数据表明,LINC00937 是瘢痕疙瘩治疗的潜在靶标。

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本文引用的文献

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Long non-coding RNA in cervical cancer: From biology to therapeutic opportunity.长链非编码 RNA 在宫颈癌中的作用:从生物学到治疗机会。
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The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models.瘢痕疙瘩疾病:异质性、组织病理学、机制与模型
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LINC00452 overexpression reverses oxLDL-induced injury of human umbilical vein endothelial cells (HUVECs) regulating miR-194-5p/IGF1R axis.LINC00452过表达通过调节miR-194-5p/IGF1R轴逆转氧化低密度脂蛋白诱导的人脐静脉内皮细胞(HUVECs)损伤。
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