Abstract
Tumor microenvironment (TME) has gradually emerged as an important research topic in the fight against cancer. The immune system is a major contributing factor in TME, and investigations have revealed that tumors are partially infiltrated with numerous immune cell subsets. We obtained transcriptome RNA-seq data from the the Cancer Genome Atlas databases for 521 patients with colon adenocarcinoma (COAD). ESTIMATE algorithms are then used to estimate the fraction of stromal and immune cells in COAD samples. A total of 1109 stromal-immune score-related differentially expressed genes were identified and used to generate a high-confidence protein-protein interaction network and univariate COX regression analysis. C-X-C motif chemokine 10 (CXCL10) was identified as the core gene by intersection analysis of data from protein-protein interaction network and univariate COX regression analysis. Then, for CXCL10, we performed gene set enrichment analysis, survival analysis and clinical analysis, and we used CIBERSORT algorithms to estimate the proportion of tumor-infiltrating immune cells in COAD samples. We discovered that CXCL10 levels could be effective for predicting the prognosis of COAD patients as well as a clue that the status of TME is transitioning from immunological to metabolic activity, which provided additional information for COAD therapies.
Highlights
In the past few years, tumor microenvironment (TME) has gradually become a hot topic in tumor research, which has important significance in the diagnosis, prevention and prognosis of tumors
Tumor metastasis is inversely proportional to immune score
1109 differentially expressed genes (DEGs) were obtained by analyzing the low-score shared genes and the high-score shared genes by intersection analysis which might be the determinant of TME status
Summary
In the past few years, tumor microenvironment (TME) has gradually become a hot topic in tumor research, which has important significance in the diagnosis, prevention and prognosis of tumors. A molecular cluster named miR-371~373 which is mainly responsible for the regulation of cancer metastasis in CRC patients has been found by Pit Ullmann et al.[3], which could help researchers develop new therapies that effectively inhibit tumor growth. Drugs targeting the MAPK signaling pathway have a limited inhibitory function on tumor growth, since it will cause the expand of NOTCH highly activated cancer cells, but if NOTCH signaling pathway is targeted, cancer cells with high MAPK activity will increase. They found that there is a high adaptability between tumor cell subpopulations, which is a mechanism that causes tumor drug resistance. The combined therapy targeting NOTCH and MAPK signaling can produce a very significant tumor suppressive effect in vivo
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