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miRSNP rs188493331：在肥厚性瘢痕和瘢痕疙瘩中 miRNA 诱导通路激活的遗传控制中的关键因素。

miRSNP rs188493331: A key player in genetic control of microRNA-induced pathway activation in hypertrophic scars and keloids.

机构信息

Department of Dermatology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, China.

Xiamen Clinical Research Center for Cancer Therapy, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, China.

出版信息

Skin Res Technol. 2024 May;30(5):e13686. doi: 10.1111/srt.13686.

DOI:10.1111/srt.13686
PMID:38682767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11057055/
Abstract

BACKGROUND

Our study aims to delineate the miRSNP-microRNA-gene-pathway interactions in the context of hypertrophic scars (HS) and keloids.

MATERIALS AND METHODS

We performed a computational biology study involving differential expression analysis to identify genes and their mRNAs in HS and keloid tissues compared to normal skin, identifying key hub genes and enriching their functional roles, comprehensively analyzing microRNA-target genes and related signaling pathways through bioinformatics, identifying MiRSNPs, and constructing a pathway-based network to illustrate miRSNP-miRNA-gene-signaling pathway interactions.

RESULTS

Our results revealed a total of 429 hub genes, with a strong enrichment in signaling pathways related to proteoglycans in cancer, focal adhesion, TGF-β, PI3K/Akt, and EGFR tyrosine kinase inhibitor resistance. Particularly noteworthy was the substantial crosstalk between the focal adhesion and PI3K/Akt signaling pathways, making them more susceptible to regulation by microRNAs. We also identified specific miRNAs, including miRNA-1279, miRNA-429, and miRNA-302e, which harbored multiple SNP loci, with miRSNPs rs188493331 and rs78979933 exerting control over a significant number of miRNA target genes. Furthermore, we observed that miRSNP rs188493331 shared a location with microRNA302e, microRNA202a-3p, and microRNA20b-5p, and these three microRNAs collectively targeted the gene LAMA3, which is integral to the focal adhesion signaling pathway.

CONCLUSIONS

The study successfully unveils the complex interactions between miRSNPs, miRNAs, genes, and signaling pathways, shedding light on the genetic factors contributing to HS and keloid formation.

摘要

背景

本研究旨在探讨肥厚性瘢痕（HS）和瘢痕疙瘩中 miRSNP- miRNA-基因-通路相互作用。

材料和方法

我们进行了一项计算生物学研究，包括差异表达分析，以鉴定 HS 和瘢痕疙瘩组织与正常皮肤相比的基因及其 mRNA，确定关键枢纽基因并丰富其功能作用，通过生物信息学全面分析 miRNA-靶基因及其相关信号通路，鉴定 MiRSNPs，并构建基于通路的网络来阐明 miRSNP-miRNA-基因-信号通路相互作用。

结果

我们的结果共揭示了 429 个枢纽基因，其在与癌症相关的蛋白聚糖、黏附斑、TGF-β、PI3K/Akt 和 EGFR 酪氨酸激酶抑制剂耐药性等信号通路中具有强烈的富集作用。特别值得注意的是，黏附斑和 PI3K/Akt 信号通路之间存在大量的串扰，使它们更容易受到 microRNAs 的调节。我们还鉴定了特定的 miRNAs，包括 miRNA-1279、miRNA-429 和 miRNA-302e，它们含有多个 SNP 位点，miRSNPs rs188493331 和 rs78979933 控制着大量 miRNA 靶基因。此外，我们观察到 miRSNP rs188493331 与 miRNA302e、miRNA202a-3p 和 miRNA20b-5p 共享位置，这三个 microRNAs 共同靶向基因 LAMA3，该基因是黏附斑信号通路的重要组成部分。

结论

本研究成功揭示了 miRSNPs、miRNAs、基因和信号通路之间的复杂相互作用，为 HS 和瘢痕疙瘩形成的遗传因素提供了新的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/4bbfa8298f92/SRT-30-e13686-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/df25096749d5/SRT-30-e13686-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/ea5ef6ddb5f0/SRT-30-e13686-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d9f1dc91e4b6/SRT-30-e13686-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/b64b156fae6d/SRT-30-e13686-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/0bc4f78065b6/SRT-30-e13686-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/9d456528ac6e/SRT-30-e13686-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d4dba9e056eb/SRT-30-e13686-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d07f0dea5069/SRT-30-e13686-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/4bbfa8298f92/SRT-30-e13686-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/df25096749d5/SRT-30-e13686-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/ea5ef6ddb5f0/SRT-30-e13686-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d9f1dc91e4b6/SRT-30-e13686-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/b64b156fae6d/SRT-30-e13686-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/0bc4f78065b6/SRT-30-e13686-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/9d456528ac6e/SRT-30-e13686-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d4dba9e056eb/SRT-30-e13686-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/d07f0dea5069/SRT-30-e13686-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b165/11057055/4bbfa8298f92/SRT-30-e13686-g003.jpg

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