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利用TCGA数据评估SMYD2蛋白在人类癌症中作用的计算方法

Computational approach for assessing the involvement of SMYD2 protein in human cancers using TCGA data.

作者信息

Yadav Arvind Kumar, Singh Tiratha Raj

机构信息

Department of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Solan-173234, Himachal Pradesh, India.

Centre of Excellence in Healthcare Technologies and Informatics (CHETI), Department of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Solan-173234, Himachal Pradesh, India.

出版信息

J Genet Eng Biotechnol. 2023 Nov 16;21(1):122. doi: 10.1186/s43141-023-00594-7.

DOI:10.1186/s43141-023-00594-7
PMID:37971632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10654300/
Abstract

BACKGROUND

SMYD2 is a protein of the SET and MYND domain-containing family SMYD. It can methylate the lysine residue of various histone and nonhistone cancer-related proteins and plays a critical role in tumorigenesis. Although emerging evidence supports the association of SMYD2 in the progression of cancers, but its definitive effect is not yet clear. Therefore, further study of the gene in relation with cancer progression needs to be conducted. In the current study, investigators used TCGA data to determine the potential carcinogenic effect of SMYD2 in 11 cancer types. The transcriptional expression, survival rate, mutations, enriched pathways, and Gene Ontology of the SMYD2 were explored using different bioinformatics tools and servers. In addition, we also examined the correlation between SMYD2 gene expression and immunocyte infiltration in multiple cancer types.

RESULTS

Findings revealed that higher expression of SMYD2 was significantly correlated with cancer incidents. In CESC and KIRC, the mRNA expression of SMYD2 was significantly correlated with overall survival (OS). In BRCA, KIRC, COAD, and HNSC, the mRNA expression of SMYD2 was significantly correlated with disease-free survival (DFS). We detected 15 missense, 4 truncating, 4 fusions, and 1 splice type of mutation. The expression of SMYD2 was significantly correlated with tumor purity and immunocyte infiltration in six cancer types. The gene GNPAT was highly associated with SMYD2. Significant pathways and Gene Ontology (GO) terms for co-expressed genes were associated to various processes linked with cancer formation.

CONCLUSION

Collectively, our data-driven results may provide reasonably comprehensive insights for understanding the carcinogenic effect of SMYD2. It suggests that SMYD2 might be used as a significant target for identifying new biomarkers for various human tumors.

摘要

背景

SMYD2是含SET和MYND结构域的SMYD家族蛋白。它可以甲基化各种组蛋白和非组蛋白癌症相关蛋白的赖氨酸残基,在肿瘤发生中起关键作用。尽管新出现的证据支持SMYD2与癌症进展有关,但其确切作用尚不清楚。因此,需要进一步研究该基因与癌症进展的关系。在本研究中,研究人员使用TCGA数据来确定SMYD2在11种癌症类型中的潜在致癌作用。使用不同的生物信息学工具和服务器探索了SMYD2的转录表达、生存率、突变、富集途径和基因本体。此外,我们还研究了多种癌症类型中SMYD2基因表达与免疫细胞浸润之间的相关性。

结果

研究结果显示,SMYD2的高表达与癌症发生显著相关。在宫颈癌(CESC)和肾透明细胞癌(KIRC)中,SMYD2的mRNA表达与总生存期(OS)显著相关。在乳腺癌(BRCA)、肾透明细胞癌、结直肠癌(COAD)和头颈部鳞状细胞癌(HNSC)中,SMYD2的mRNA表达与无病生存期(DFS)显著相关。我们检测到15种错义突变、4种截短突变、4种融合突变和1种剪接型突变。SMYD2的表达与六种癌症类型中的肿瘤纯度和免疫细胞浸润显著相关。基因GNPAT与SMYD2高度相关。共表达基因的重要途径和基因本体(GO)术语与癌症形成相关的各种过程有关。

结论

总体而言,我们的数据驱动结果可能为理解SMYD2的致癌作用提供相当全面的见解。这表明SMYD2可能作为识别各种人类肿瘤新生物标志物的重要靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/45bd45cddc50/43141_2023_594_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/880cef898a39/43141_2023_594_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/4ba89a9a21b2/43141_2023_594_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/efa497d90ae8/43141_2023_594_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/50f1018976a9/43141_2023_594_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/9e313fb0a82d/43141_2023_594_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/6046456683b2/43141_2023_594_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/410f15cf73f5/43141_2023_594_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/253bc5f09949/43141_2023_594_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/45bd45cddc50/43141_2023_594_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/880cef898a39/43141_2023_594_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/4ba89a9a21b2/43141_2023_594_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/efa497d90ae8/43141_2023_594_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/50f1018976a9/43141_2023_594_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/9e313fb0a82d/43141_2023_594_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/6046456683b2/43141_2023_594_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/410f15cf73f5/43141_2023_594_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/253bc5f09949/43141_2023_594_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc78/10654300/45bd45cddc50/43141_2023_594_Fig9_HTML.jpg

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