Results of GO KEGG enrichment analysis.
<div><p>Backgrounds</p><p><i>KLKs</i> have been proved to be key regulators of the tumor microenvironment. In this study, we explored the potential of <i>Kallikrein-related peptidases</i> (<i>KLKs</i>) as clinical diagnostic and prognostic markers in patients with kidney renal clear cell carcinoma (KIRC) as well as their relationship with common immuno-inhibitor and immune cell infiltration in the tumor microenvironment to provide new targets and novel ideas for KIRC therapy.</p><p>Methods</p><p>Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), UCSC Xena, Genotype-Tissue Expression (GTEx), Kaplan-Meier plotter, cBioPortal, STRING, GeneMANIA, and TISIDB were used to analyze the differential expression, prognostic value, gene changes, molecular interaction, and immune infiltration of <i>KLKs</i> in patients with KIRC.</p><p>Results</p><p>From the gene expression level, it can be determined that <i>KLK1</i>, <i>KLK6</i>, and <i>KLK7</i> are differentially expressed in KIRC and normal tissues. From the perspective of clinical prognosis, <i>KLK1</i>, <i>KLK13</i>, and <i>KLK14</i> are highly correlated with the clinical prognosis of KIRC. The expression of <i>KLKs</i> is regulated by various immunosuppressive agents, with KDR, PVRL2, and VTCN1 being the most significant. The expression of <i>KLKs</i> is significantly correlated with the infiltration of various immune cells, of which Eosinophils and Neutrophils are the most significant.</p><p>Conclusions</p><p><i>KLK1</i>, <i>KLK6</i>, <i>KLK7</i>, <i>KLK13</i>, and <i>KLK14</i> have potential as diagnostic and prognostic biomarkers, among which <i>KLK1</i> is the most significant. This study may provide detailed immune information and promising targets for KIRC immunotherapy to assist in designing new immunotherapies.</p></div>
Publication Details
- Journal
- Figshare
- Published
- 2024-08-08
- DOI
- https://doi.org/10.1371/journal.pone.0305070.s001
- Primary Topic
- Mycorrhizal Fungi and Plant Interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00