# CSDE1 depletion inhibits tumor progression through enhancing B-cell infiltration in NSCLC

## TL;DR

This study shows that reducing CSDE1 in lung cancer slows tumor growth by boosting B-cell presence in the tumor environment.

## Contribution

The novel finding is that CSDE1 depletion enhances B-cell infiltration and humoral immunity, offering a new target for cancer immunotherapy.

## Key findings

- CSDE1 deletion in mice significantly inhibits tumor growth in vivo.
- CSDE1 knockout increases tumor-infiltrating B lymphocytes and B-cell-mediated immunity.
- B-cell depletion reverses the tumor-inhibitory effect of CSDE1 deletion, highlighting B cells' critical role.

## Abstract

Although most immunotherapy research focuses on T cells, increasing evidence highlights the significant role of tumor-infiltrating B lymphocytes (TIL-Bs) in cancer therapy. CSDE1 has been implicated in various cancers and immune responses. This study investigates the role of CSDE1 in lung cancer progression and its impact on the tumor immune microenvironment. We found that CSDE1 promotes lung cancer progression in vivo but not in vitro. Using the tumor-bearing mice model with Csde1 knockout, we demonstrated that Csde1 deletion significantly inhibited tumor growth. Single-cell RNA sequencing revealed that Csde1 knockout reshaped the tumor immune microenvironment, particularly by significantly increasing TIL-B levels, a finding confirmed by flow cytometry and immunofluorescence. Moreover, Csde1 knockout enhanced B-cell-mediated humoral immunity. Notably, depleting B cells in Csde1 knockout mice reversed the inhibitory effect of Csde1 deletion on tumor progression, underscoring the critical role of B cells in this process. These findings suggest that CSDE1 facilitates tumor progression by modulating TIL-Bs and the broader immune microenvironment. This study provides a new potential target and valuable insights into tumor immunotherapy, emphasizing the importance of B cells in cancer treatment strategies.