Please login first
Expression of Tryptophanyl-tRNA Synthetase (WARS) and Indoleamine 2,3-Dioxygenase-1 (IDO1) in the Prediction of Bladder Cancer Staging
* , , ,
1  Uninove, department of biotechnology. 235/249 Vergueiro Street, Liberdade - São Paulo - SP Brazil, Zip Code 01525-000.
Academic Editor: Paola Saccomandi

Abstract:

Introduction

Bladder cancer (BC) is one of the most common neoplasms in the world. Like other types, BC can produce the enzyme indoleamine 2,3-dioxygenase-1 (IDO1), which, by modulating the immune system, protects the tumor and favors its progression. When present, IDO1 degrades tryptophan in the microenvironment, producing kynurenine catabolites. This situation blocks the local immune response but does not affect the IDO1-producing cell itself. The mechanisms for this resistance remain unknown, but there is evidence that reserves are generated by the enzyme tryptophanyl-tRNA synthetase (WARS), which loads tRNA with the amino acid, ensuring protein synthesis and the cell cycle.

The objective of this study was to verify if the expression of IDO1 and WARS is associated with BC staging.

Materials and Methods

The study included BC specimens extracted from 165 patients, 88 with non-muscle invasive BC (NMIBC) and 77 with muscle invasive BC (MIBC). The project was approved by the ethics committee (49446515.0.0000.5511). The expression of IDO1 and WARS was evaluated by immunohistochemistry in both neoplastic and inflammatory cells. Correlation analysis (Spearman) and ROC curve were used.

Preliminary Results

Although no correlation was detected between IDO1 and WARS, the expression of both proteins was effective in predicting NMIBC.

Preliminary Conclusion

It is possible that the enzymes IDO1 and WARS play a role in the pathophysiology of BC and have predictive power in disease staging. This study is ongoing for further clarification.

Funding

FAPESP 2022/15575-8

Keywords: Bladder cancer, Immunomodulation, Tryptophan catabolism
Comments on this paper
Currently there are no comments available.



 
 
Top