Characterization of a Tumor-Microenvironment-Relevant Gene Set Based on Tumor Severity in Colon Cancer and Evaluation of Its Potential for Dihydroartemisinin Targeting

Colon cancer (COAD) is a leading cause of cancer mortality in the world. Most patients with COAD die as a result of cancer cell metastasis. However, the mechanisms underlying the metastatic phenotype of COAD remain unclear. Instead, particular features of the tumor microenvironment (TME) could predi...

Full description

Saved in:
Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2021, Vol.2021, p.1-10
Main Authors: Liang, Bo, Zheng, Biao, Zhou, Yan, Lai, Zheng-Quan, Zhang, Citing, Yan, Zilong, Li, Zhangfu, Li, Xuefei, Gong, Peng, Qu, Jianhua, Liu, Jikui
Format: Article
Language:English
Subjects:
Alternative medicine
Biomarkers
Cancer therapies
Clinical outcomes
Colon cancer
Colorectal cancer
Correlation analysis
Dihydroartemisinin
Gene expression
Infiltration
Investigations
Ligands
Medical prognosis
Metastases
Molecular modelling
Ontology
Phenotypes
Proteins
Servers
Survival analysis
Tumor microenvironment
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Colon cancer (COAD) is a leading cause of cancer mortality in the world. Most patients with COAD die as a result of cancer cell metastasis. However, the mechanisms underlying the metastatic phenotype of COAD remain unclear. Instead, particular features of the tumor microenvironment (TME) could predict adverse outcomes including metastasis in patients with COAD, and the role of TME in governing COAD progression is undeniable. Therefore, exploring the role of TME in COAD may help us better understand the molecular mechanisms behind COAD progression which may improve clinical outcomes and quality of patients. Here, we identified a Specific TME Regulatory Network including AEBP1, BGN, POST, and FAP (STMERN) that is highly involved in clinical outcomes of patients with COAD. Comprehensive in silico analysis of our study revealed that the STMERN is highly correlated with the severity of COAD. Meanwhile, our results reveal that the STMERN might be associated with immune infiltration in COAD. Importantly, we show that dihydroartemisinin (DHA) potentially interacts with the STMERN. We suggest that DHA might contribute to immune infiltration through regulating the STMERN in COAD. Taken together, our data provide a set of biomarkers of progression and poor prognosis in COAD. These findings could have potential prognostic and therapeutic implications in the progression of COAD.
ISSN:1741-427X
1741-4288
DOI:10.1155/2021/4812068