# PROM1 and EFTUD2 Expression in High-Grade Clear Cell Renal Cell Carcinoma as a Molecular Marker for Survival Rate

## TL;DR

This study explores how the proteins PROM1 and EFTUD2 relate to survival rates in high-grade clear cell kidney cancer, suggesting they could be important for diagnosis and treatment.

## Contribution

The study identifies EFTUD2 and PROM1 as potential molecular markers for survival in high-grade clear cell renal cell carcinoma.

## Key findings

- EFTUD2 expression is significantly associated with progression-free survival in ccRCC patients.
- PROM1 is downregulated in ccRCC, potentially affecting cell surface interactions.
- Protein expression heterogeneity within tumors highlights the need for nuanced understanding of EFTUD2's role.

## Abstract

Clear cell renal cell carcinoma (ccRCC) is a significant global cancer, particularly impacting individuals in Western countries. Despite that, the molecular mechanisms driving renal cell carcinoma progression remain poorly understood, highlighting the need to investigate these mechanisms and identify novel therapeutic targets. Literature evidence suggests that elongation factor Tu GTP binding domain containing 2 (EFTUD2) and prominin (PROM1) gene expression have significant diagnostic potential in early tumor detection, potentially reflecting the trends in progression, and may become a novel therapeutic target. Therefore, this study aimed to evaluate EFTUD2 and PROM1 protein expression on clinical characteristics of ccRCC patients, especially overall and progression-free survival. To achieve that goal, we have combined publicly available liquid chromatography–mass spectrometry (LC-MS/MS) protein expression data with a comprehensive literature review to identify key protein markers for further study and immunohistochemical (IHC) analysis. Our findings highlight the importance of considering protein expression heterogeneity within tumors. The significant variation in EFTUD2 expression, its association with PFS, and its intricate connections with the mRNA splicing machinery underscore the need for a more nuanced understanding of its role in ccRCC. Similarly, the downregulation of PROM1 and its potential effects on cell surface interactions warrant further exploration. Future studies should focus on elucidating the mechanisms underlying these observations, exploring their potential as therapeutic targets, and investigating the specific pathways affected by their dysregulation.