4.6 Article

LncRNA expression profiles and validation in keloid and normal skin tissue

期刊

INTERNATIONAL JOURNAL OF ONCOLOGY
卷 47, 期 5, 页码 1829-1838

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2015.3177

关键词

keloid; lncRNA; gene expression; calcium channel; CACNA1G-AS1

类别

资金

  1. National Natural Science Foundation of China (NSFC) [81071571]

向作者/读者索取更多资源

Keloid is a type of pathological skin scar. Pathogenesis of keloid is complex and is not fully understood. LncRNA can regulate gene expression on different levels. It also participates in cell cycle regulation and cell proliferation. The present study investigated the potential biological function of IncRNA in keloid. We identified differential expression of lncRNAs and mRNAs between 3 pairs of keloid and normal skin tissue by microarray. Differentially expressed lncRNAs were validated by quantitative reverse transcriptase-PCR (qRT-PCR). Gene Ontology (GO) and pathway analysis presented the characteristics of associated protein-coding genes. Additionally, a co-expression network of lncRNA and mRNA was constructed to find potential underlying regulation targets. There were 1,731 IncRNAs constantly upregulated and 782 downregulated, 1,079 mRNAs upregulated and 3,282 downregulated in keloid respectively (fold change 2.0, P<0.05). We chose, respectively, 3 upregulated and 1 downregulated lncRNA for qRT-PCR and results were consistent with microarray. Moreover, 11 pathways were related with upregulated transcripts and 44 with downregulated in keloid. The co-expression network revealed that one lncRNA was connected with numerous mRNAs, and vice versa. Furthermore, bioinformation analysis suggested that lncRNA CACNA1G-AS1 may be crucial to keloid formation. In conclusion, groups of lncRNAs were aberrantly expressed in keloid compared with normal skin tissue, which indicated that differentially expressed IncRNAs may play a key role in keloid formation. The present study provides new insights into keloid pathology and potential targets for treatment of keloid.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据