Abstract

Background

Motile Sperm Domain-Containing Protein 1 (MOSPD1) has been implicated in breast cancer (BC) pathophysiology, but its exact role remains unclear. This study aimed to assess MOSPD1 expression levels in BC versus normal tissues and investigate its diagnostic potential.

Methods

MOSPD1 expression was analyzed in BC and normal tissues, with Receiver Operating Characteristic analysis for diagnostic evaluation. Validation was performed using immunohistochemistry. Functional studies included tumor growth assays, MOSPD1 suppression and overexpression experiments, and testing BC cell responses to anti-PD-L1 therapy.

Results

MOSPD1 expression was significantly higher in BC samples than normal tissues, correlating with poor clinical outcomes in BC patients. MOSPD1 suppression inhibited tumor growth, while overexpression accelerated it. Silencing MOSPD1 enhanced BC cell sensitivity to anti-PD-L1 therapy and decreased Th2 cell activity. In vivo experiments supported these findings, showing the impact of MOSPD1 on tumor growth and response to therapy.

Conclusions

Elevated MOSPD1 levels in BC suggest its potential as a biomarker for adverse outcomes. Targeting MOSPD1, particularly with anti-PD-L1 therapy, may effectively inhibit BC tumor growth and modulate immune responses. This study emphasizes the significance of MOSPD1 in BC pathophysiology and highlights its promise as a therapeutic target.

Details

Title
Deciphering MOSPD1’s impact on breast cancer progression and therapeutic response
Author
Jiang, Yiling; Li, Hailong; Jiang, Sixuan Wuohong; Zeng, Lijun; Tang, Yuanbin; Luo, Lunqi; Ouyang, Lianjie; Du, Wei; Li, Yuehua
Pages
1-21
Section
Research
Publication year
2024
Publication date
2024
Publisher
BioMed Central
e-ISSN
1745-6150
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3115132236
Copyright
© 2024. This work is licensed under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.