Deciphering MOSPD1's impact on breast cancer progression and therapeutic response.

Biol Direct

Department of Oncology, The First Affiliated Hospital, Hengyang Medical School, University of South China, No. 69 Chuanshan Road, Hengyang, Hunan Province, 421001, People's Republic of China.

Published: October 2024

AI Article Synopsis

  • MOSPD1 is found to be overexpressed in breast cancer (BC) tissues compared to normal tissues, indicating a possible role in cancer progression and poor patient outcomes.
  • Functional experiments demonstrated that reducing MOSPD1 levels inhibited tumor growth and improved the effectiveness of anti-PD-L1 therapy in BC cells.
  • The study suggests that MOSPD1 could serve as a biomarker for negative clinical outcomes and a potential therapeutic target to enhance treatment responses in patients with breast cancer.

Article 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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11453086PMC
http://dx.doi.org/10.1186/s13062-024-00531-9DOI Listing

Publication Analysis

Top Keywords

tumor growth
16
mospd1 expression
12
normal tissues
12
mospd1
11
breast cancer
8
mospd1 suppression
8
anti-pd-l1 therapy
8
deciphering mospd1's
4
mospd1's impact
4
impact breast
4

Similar Publications

Bladder cancer (BC) is the tenth most common tumor worldwide, characterized by high incidence rates and mortality. This study aimed to explore the role of Methyltransferase like 13 (METTL13) in BC cells. J82 and T24 cells were cultured for experiments.

View Article and Find Full Text PDF

This study attempted to identify the relevant pathways involved in autophagy activation of pancreatic cancer and explore the mechanisms underlying immune evasion. Western blot (WB) was used to detect the expression of ITGB4, BNIP3, autophagy-related proteins and MHC-I. Co-immunoprecipitation (Co-IP) was used to verify the binding mode of ITGB4 and BNIP3.

View Article and Find Full Text PDF

In this study, we discovered and identified a novel AXL/triple angiokinase inhibitor by rational structural modification based on the structure of triple angiokinase inhibitor Nintedanib. We found that potently inhibited AXL expression with the IC value of 3.75 nM and possessed similar inhibitory activity on KDR as Nintedanib.

View Article and Find Full Text PDF

Glioblastoma (GBM) is the most frequent malignant brain tumor. We recently discovered that oncolytic herpes simplex virus engineered to disable tumor-intrinsic protein kinase R (PKR) signaling (oHSV-shPKR) could increase oHSV oncolysis and anti-tumor immune response. However, here we show that disabling tumor-intrinsic PKR signaling can also induce the activation of the indoleamine 2,3-dioxygenase (IDO) signaling pathway.

View Article and Find Full Text PDF

Inhibitory Effect of PRMT5/MTA Inhibitor on MTAP-Deficient Glioma May Be Influenced by Surrounding Normal Cells.

Cancer Med

December 2024

School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, People's Republic of China.

Background: Methylthioadenosine phosphorylase (MTAP) and protein arginine methyltransferase 5 (PRMT5) are considered to be a synthetic lethal pair of targets, due to the fact that deletion of MTAP leads to massive production of methylthioadenosine (MTA) decreasing the activity of PRMT5. In vitro and in vivo experiments have demonstrated that MRTX1719, a small molecule that selectively binds PRMT5/MTA complex, significantly inhibits the proliferation of MTAP-deficient tumors and has a weak toxic effect on normal cells. However, it has been reported that MTAP-deleted tumors did not significantly accumulate MTA in vivo due to metabolism of MTA by MTAP-expressing stroma, which might lead to a diminished anti-cancer effect of MRTX1719.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!