Last update 01 Nov 2024

MS4A4A

Last update 01 Nov 2024

Basic Info

Synonyms

4SPAN1, CD20 antigen-like 1, CD20L1

+ [6]

Introduction

May be involved in signal transduction as a component of a multimeric receptor complex.

Drugs associated with MS4A4A

CN116789821

Patent Mining

Target

MS4A4A

Mechanism-

Active Org.

Southern Hospital of Southern Medical University

Originator Org.

Southern Hospital of Southern Medical University

Active Indication

Gastrointestinal Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AL0-44

Target

MS4A4A

Mechanism

MS4A4 gene modulators

Active Org.-

Originator Org.

Alector, Inc.

Active Indication-

Inactive Indication

Alzheimer Disease

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1299

Target

MS4A4A

Mechanism

MS4A4 gene modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Immune System Diseases [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MS4A4A

100 Translational Medicine associated with MS4A4A

0 Patents (Medical) associated with MS4A4A

Literatures (Medical) associated with MS4A4A

01 Sep 2024·CNS Neuroscience & Therapeutics

Correction to Targeting MS4A4A: A novel pathway to improve immunotherapy responses in glioblastoma

01 Jul 2024·CNS Neuroscience & Therapeutics

Targeting MS4A4A: A novel pathway to improve immunotherapy responses in glioblastoma

Article

Author: Li, Nu ; Cui, Xiangguo ; Wang, Yiliang ; Li, Chuanyu ; Luo, Shuyan ; Jiang, Yu ; Shao, Guangcai ; Li, Xiang ; Cai, Dasheng

AbstractIntroductionGlioblastoma (GBM) remains a challenging brain tumor to treat, with limited response to PD‐1 immunotherapy due to tumor‐associated macrophages (TAMs), specifically the M2 phenotype. This study explores the potential of MS4A4A (membrane spanning four domains, subfamily A, member 4A) inhibition in driving M2 macrophage polarization toward the M1 phenotype via the ferroptosis pathway to enhance the effectiveness of immunotherapy in GBM.MethodsSingle‐cell RNA sequencing and spatial transcriptomic analyses were employed to characterize M2 macrophages and MS4A4A expression in GBM. In vitro studies utilizing TAM cultures, flow cytometry, and western blot validations were conducted to assess the impact of MS4A4A on the tumor immune microenvironment and M2 macrophage polarization. In vivo models, including subcutaneous and orthotopic transplantation in mice, were utilized to evaluate the effects of MS4A4A knockout and combined immune checkpoint blockade (ICB) therapy on tumor growth and response to PD‐1 immunotherapy.ResultsDistinct subsets of GBM‐associated macrophages were identified, with spatial distribution in tumor tissue elucidated. In vivo experiments demonstrated that inhibiting MS4A4A and combining ICB therapy effectively inhibited tumor growth, reshaped the tumor immune microenvironment by reducing M2 TAM infiltration and enhancing CD8+ T‐cell infiltration, ultimately leading to complete tumor eradication.ConclusionMS4A4A inhibition shows promise in converting M2 macrophages to M1 phenotype via ferroptosis, decreasing M2‐TAM infiltration, and enhancing GBM response to PD‐1 immunotherapy. These findings offer a novel approach to developing more effective immunotherapeutic strategies for GBM.

01 May 2024·Clinical and Translational Medicine

Integrating single‐cell and spatial analysis reveals MUC1‐mediated cellular crosstalk in mucinous colorectal adenocarcinoma

Article

Author: Lin, Jiayi ; Zhang, Jing ; Hu, Hao ; Zhou, Haiyang ; Shen, Yiwen ; Zheng, Guangyong ; Luan, Xin ; Liu, Sanhong ; Zhang, Beibei ; Zhang, Weidong ; Wang, Anqi

AbstractBackgroundMucinous colorectal adenocarcinoma (MCA) is a distinct subtype of colorectal cancer (CRC) with the most aggressive pattern, but effective treatment of MCA remains a challenge due to its vague pathological characteristics. An in‐depth understanding of transcriptional dynamics at the cellular level is critical for developing specialised MCA treatment strategies.MethodsWe integrated single‐cell RNA sequencing and spatial transcriptomics data to systematically profile the MCA tumor microenvironment (TME), particularly the interactome of stromal and immune cells. In addition, a three‐dimensional bioprinting technique, canonical ex vivo co‐culture system, and immunofluorescence staining were further applied to validate the cellular communication networks within the TME.ResultsThis study identified the crucial intercellular interactions that engaged in MCA pathogenesis. We found the increased infiltration of FGF7+/THBS1+ myofibroblasts in MCA tissues with decreased expression of genes associated with leukocyte‐mediated immunity and T cell activation, suggesting a crucial role of these cells in regulating the immunosuppressive TME. In addition, MS4A4A+ macrophages that exhibit M2‐phenotype were enriched in the tumoral niche and high expression of MS4A4A+ was associated with poor prognosis in the cohort data. The ligand‐receptor‐based intercellular communication analysis revealed the tight interaction of MUC1+ malignant cells and ZEB1+ endothelial cells, providing mechanistic information for MCA angiogenesis and molecular targets for subsequent translational applications.ConclusionsOur study provides novel insights into communications among tumour cells with stromal and immune cells that are significantly enriched in the TME during MCA progression, presenting potential prognostic biomarkers and therapeutic strategies for MCA.Key points

Tumour microenvironment profiling of MCA is developed.

MUC1+ tumour cells interplay with FGF7+/THBS1+ myofibroblasts to promote MCA development.

MS4A4A+ macrophages exhibit M2 phenotype in MCA.

ZEB1+ endotheliocytes engage in EndMT process in MCA.

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MS4A4A

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