Cancer-associated fibroblasts (CAFs) based model reveals potential for predicting bladder cancer patients’ prognoses and immunotherapy responses

Author:

Dong Mengyuan,Zhang Xu

Abstract

Aim: The purpose of this study is to enhance the understanding of bladder cancer and the role of cancer-associated fibroblasts (CAFs) in its progression. We aim to identify CAF-specific biomarkers and develop a prognostic prediction model based on CAFs, thereby contributing to the advancement of treatment strategies and the identification of prognostic and predictive biomarkers for bladder cancer. Method: We employed single-cell RNA sequencing to detect biomarkers for CAFs in bladder cancer cells. Bladder cancer cohorts were categorized into low- and high-CAF groups using the ssGSEA algorithm. The study also explored the association between CAF-related scores, immune-related cells, and immune checkpoint-related genes. Furthermore, we performed GSVA analysis to understand the biological features of CAFs and their link to various cancer-related pathways. Result: Ten genes were identified as CAF markers in bladder cancer cells. A significant difference was found with 2712 differentially expressed genes between low-CAF and high-CAF tissues. The CAFs-based prognostic prediction model included nine genes (ALDH1L2, AL450384.2, EMP1, LINC02362, WFIKKN1, GOLGA8A, POU5F1, AL354919.2, PTPRR), which are potentially crucial in predicting bladder cancer prognosis. The GSVA analysis revealed the involvement of several cancer-related pathways, such as WNT, toll-like receptor, TGF-beta, MAPK, and MTOR signaling pathways, in the CAFs-based prognostic model. Conclusion: This study highlights the significant role of CAFs in the progression and prognosis of bladder cancer. The identified CAF biomarkers and the constructed prognostic model provide valuable insights for future research and potential therapeutic targets. CAF-dependent pathways are promising for the development of new treatments and improving the prognosis of bladder cancer patients.

Publisher

OAE Publishing Inc.

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