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与皮肤鳞状细胞癌进展相关的重要生物标志物的鉴定

Significant Biomarkers Identification Associated with Cutaneous Squamous Cell Carcinoma Progression.

作者信息

Qiu Cheng-Gang, Shen Bin, Sun Xiao-Qi

机构信息

Department of Burn, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, 311200, Zhejiang, People's Republic of China.

Department of Plastic Surgery, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, 311200, Zhejiang, People's Republic of China.

出版信息

Int J Gen Med. 2022 Mar 2;15:2347-2360. doi: 10.2147/IJGM.S357022. eCollection 2022.

DOI:10.2147/IJGM.S357022
PMID:35264873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8901050/
Abstract

BACKGROUND

This study aimed to identify significant genes associated with cutaneous squamous cell carcinoma (CSCC) initiation and development.

METHODS

The overlapped differential expressed genes (DEGs) between normal and CSCC samples were firstly screened out, followed by KEGG analysis. The top 10 hub genes were then detected from the whole protein-protein interaction (PPI) network. Further, important biomarkers continuously associated with actinic keratosis (AK), CSCC, and CSCC invasion was successively filtrated. GSEA analysis was finally performed to reveal potential mechanisms associated with biomarkers.

RESULTS

A total of 179 DEGs were identified, which were enriched in pathways in cancer, PI3K-Akt signaling pathway, and human papillomavirus infection. The 10 hub genes were firstly identified from the PPI network, and they were all highly expressed in AK tissues compared with normal tissues. Next, we found that 6 genes were overexpressed in CSCC compared with AK tissues. Further, we identified that the expression of 2 genes (MYBL2 and TK1) was higher in CSCC invasion groups compared with samples without invasion. Through a series of filtrations, we confirmed that MYBL2 and TK1 were the most significant biomarkers associated with CSCC initiation and progression. The pan-cancer analysis further supported their prognostic value in human cancers. GSEA analysis found that they positively correlated with N glycan biosynthesis and p53 signaling pathways.

CONCLUSION

MYBL2 and TK1 were proved to play a vital role in CSCC tumorigenesis and progression, which may act as promising biomarkers or therapeutic targets for accurate diagnosis and treatment of CSCC.

摘要

背景

本研究旨在鉴定与皮肤鳞状细胞癌(CSCC)起始和发展相关的重要基因。

方法

首先筛选出正常样本与CSCC样本之间的重叠差异表达基因(DEG),随后进行KEGG分析。然后从整个蛋白质-蛋白质相互作用(PPI)网络中检测出前10个枢纽基因。此外,依次筛选出与光化性角化病(AK)、CSCC及CSCC侵袭持续相关的重要生物标志物。最后进行基因集富集分析(GSEA)以揭示与生物标志物相关的潜在机制。

结果

共鉴定出179个DEG,这些基因富集于癌症通路、PI3K-Akt信号通路和人乳头瘤病毒感染。首先从PPI网络中鉴定出10个枢纽基因,与正常组织相比,它们在AK组织中均高表达。接下来,我们发现与AK组织相比,6个基因在CSCC中过表达。进一步地,我们鉴定出与无侵袭样本相比,2个基因(MYBL2和TK1)在CSCC侵袭组中表达更高。通过一系列筛选,我们证实MYBL2和TK1是与CSCC起始和进展相关的最显著生物标志物。泛癌分析进一步支持了它们在人类癌症中的预后价值。GSEA分析发现它们与N-聚糖生物合成和p53信号通路呈正相关。

结论

已证明MYBL2和TK1在CSCC肿瘤发生和进展中起关键作用,它们可能作为有前景的生物标志物或治疗靶点用于CSCC的准确诊断和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/890350fb337b/IJGM-15-2347-g0012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/20b41fc10d24/IJGM-15-2347-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/f0232c67d28c/IJGM-15-2347-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/8319c65d808d/IJGM-15-2347-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/af9e5cf77315/IJGM-15-2347-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/bb2f8e8b892b/IJGM-15-2347-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/96b3001e831d/IJGM-15-2347-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/70e6c070b9f6/IJGM-15-2347-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/61eb1e32e3ee/IJGM-15-2347-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/68c5f969eb8b/IJGM-15-2347-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/14c59e48e535/IJGM-15-2347-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/089be308749d/IJGM-15-2347-g0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/890350fb337b/IJGM-15-2347-g0012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/20b41fc10d24/IJGM-15-2347-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/f0232c67d28c/IJGM-15-2347-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/8319c65d808d/IJGM-15-2347-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/af9e5cf77315/IJGM-15-2347-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/bb2f8e8b892b/IJGM-15-2347-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/96b3001e831d/IJGM-15-2347-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/70e6c070b9f6/IJGM-15-2347-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/61eb1e32e3ee/IJGM-15-2347-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/68c5f969eb8b/IJGM-15-2347-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/14c59e48e535/IJGM-15-2347-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/089be308749d/IJGM-15-2347-g0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/858e/8901050/890350fb337b/IJGM-15-2347-g0012.jpg

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