# Analysis of CacyBP/SIP, ERK1/2, and p38 Expression in Low‐ and High‐Grade Papillary Urothelial Carcinoma

## TL;DR

This study examines the expression of CacyBP/SIP, ERK1/2, and p38 in low- and high-grade bladder cancer to understand their roles in cancer progression.

## Contribution

The study identifies CacyBP/SIP as a potential driver of urothelial carcinoma by modulating ERK1/2 and p38 activity.

## Key findings

- CacyBP/SIP gene expression was strongest in high-grade tumor tissues, mainly in the nucleus.
- p38 kinase expression was elevated in tumor tissues, while ERK1/2 expression was reduced.
- CacyBP/SIP may contribute to urothelial carcinoma progression by affecting ERK1/2 and p38 activity.

## Abstract

Papillary urothelial carcinoma (transitional cell carcinoma) is one of the most common malignant tumors of the urinary tract. Urothelial carcinomas are classified into muscle‐invasive and non‐muscle‐invasive types. Among the latter, papillary urothelial carcinoma is further categorized into low‐grade and high‐grade forms. The aggressiveness of bladder cancer depends on the stage and grade of the disease. The CacyBP/SIP protein and MAP kinases play key roles in various cellular processes and signaling pathways that determine cell survival or death. This study aimed to assess the expression of CacyBP/SIP, ERK1/2, and p38 in low‐ and high‐grade papillary urothelial carcinoma using immunohistochemical and molecular analyses.

Tissue samples were obtained from 20 patients with high‐grade urothelial carcinoma and 20 patients with low‐grade urothelial carcinoma. Adjacent non‐cancerous tissues served as comparative controls. Immunohistochemistry and qRT‐PCR were used to evaluate the expression of CacyBP/SIP, ERK1/2, and p38.

The strongest expression of the CacyBP/SIP gene was observed in tumor tissues with high malignant potential, predominantly in the nuclear compartment. Similarly, p38 kinase expression was elevated, whereas ERK1/2 expression was reduced in bladder tumor tissues compared to adjacent normal bladder tissues.

These findings suggest that CacyBP/SIP may play a critical role in urothelial carcinoma progression by modulating ERK1/2 and p38 kinase activity.