# An integrated bioinformatic investigation of kallikrein gene family members in kidney renel cell carcinoma

**Authors:** Baoquan Wang, Lun Yang, Haiyun Qin, Fengzhen Li, Peitong Zhang, Gurudeeban Selvaraj, Gurudeeban Selvaraj, Gurudeeban Selvaraj, Gurudeeban Selvaraj

PMC · DOI: 10.1371/journal.pone.0305070 · PLOS ONE · 2024-08-08

## TL;DR

This study explores how specific kallikrein genes relate to kidney cancer and immune responses, offering new diagnostic and treatment ideas.

## Contribution

Identifies KLK1, KLK6, KLK7, KLK13, and KLK14 as potential biomarkers for kidney cancer prognosis and immunotherapy.

## Key findings

- KLK1, KLK6, and KLK7 show differential expression in kidney cancer tissues compared to normal tissues.
- KLK1, KLK13, and KLK14 are strongly linked to clinical prognosis in kidney cancer patients.
- KLK expression correlates with immune cell infiltration, particularly Eosinophils and Neutrophils.

## Abstract

KLKs have been proved to be key regulators of the tumor microenvironment. In this study, we explored the potential of Kallikrein-related peptidases (KLKs) 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.

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 KLKs in patients with KIRC.

From the gene expression level, it can be determined that KLK1, KLK6, and KLK7 are differentially expressed in KIRC and normal tissues. From the perspective of clinical prognosis, KLK1, KLK13, and KLK14 are highly correlated with the clinical prognosis of KIRC. The expression of KLKs is regulated by various immunosuppressive agents, with KDR, PVRL2, and VTCN1 being the most significant. The expression of KLKs is significantly correlated with the infiltration of various immune cells, of which Eosinophils and Neutrophils are the most significant.

KLK1, KLK6, KLK7, KLK13, and KLK14 have potential as diagnostic and prognostic biomarkers, among which KLK1 is the most significant. This study may provide detailed immune information and promising targets for KIRC immunotherapy to assist in designing new immunotherapies.

## Linked entities

- **Genes:** KLK1 (kallikrein 1) [NCBI Gene 3816], KLK6 (kallikrein related peptidase 6) [NCBI Gene 5653], KLK7 (kallikrein related peptidase 7) [NCBI Gene 5650], KLK13 (kallikrein related peptidase 13) [NCBI Gene 26085], KLK14 (kallikrein related peptidase 14) [NCBI Gene 43847], KDR (kinase insert domain receptor) [NCBI Gene 3791], NECTIN2 (nectin cell adhesion molecule 2) [NCBI Gene 5819], VTCN1 (V-set domain containing T cell activation inhibitor 1) [NCBI Gene 79679]

## Full-text entities

- **Genes:** KLK1 (kallikrein 1) [NCBI Gene 3816] {aka KLKR, Klk6, hK1}, KLK6 (kallikrein related peptidase 6) [NCBI Gene 5653] {aka Bssp, Klk7, PRSS18, PRSS9, SP59, hK6}, KDR (kinase insert domain receptor) [NCBI Gene 3791] {aka CD309, FLK1, VEGFR, VEGFR2}, NECTIN2 (nectin cell adhesion molecule 2) [NCBI Gene 5819] {aka CD112, HVEB, PRR2, PVRL2, PVRR2}, KLK7 (kallikrein related peptidase 7) [NCBI Gene 5650] {aka PRSS6, SCCE, hK7}, KLK13 (kallikrein related peptidase 13) [NCBI Gene 26085] {aka KLK-L4, KLKL4}, VTCN1 (V-set domain containing T cell activation inhibitor 1) [NCBI Gene 79679] {aka B7-H4, B7H4, B7S1, B7X, B7h.5, PRO1291}, KLK14 (kallikrein related peptidase 14) [NCBI Gene 43847] {aka KLK-L6}
- **Diseases:** tumor (MESH:D009369), KIRC (MESH:D002292)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11309392/full.md

## References

44 references — full list in the complete paper: https://tomesphere.com/paper/PMC11309392/full.md

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Source: https://tomesphere.com/paper/PMC11309392