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Updated: Jul 25, 2025

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Targeting cGAS/STING signaling-mediated myeloid immune cell dysfunction in TIME
Vijay Kumar1, Caitlin Bauer2, John H Stewart3,4,5
1Department of Interdisciplinary Oncology, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, New Orleans, LA, 70012, USA. vkuma2@lsuhsc.edu.
Abstract:
Myeloid immune cells (MICs) are potent innate immune cells serving as first responders to invading pathogens and internal changes to cellular homeostasis. Cancer is a stage of altered cellular homeostasis that can originate in response to different pathogens, chemical carcinogens, and internal genetic/epigenetic changes. MICs express several pattern recognition receptors (PRRs) on their membranes, cytosol, and organelles, recognizing systemic, tissue, and organ-specific altered homeostasis. cGAS/STING signaling is a cytosolic PRR system for identifying cytosolic double-stranded DNA (dsDNA) in a sequence-independent but size-dependent manner. The longer the cytosolic dsDNA size, the stronger the cGAS/STING signaling activation with increased type 1 interferon (IFN) and NF-κB-dependent cytokines and chemokines' generation. The present article discusses tumor-supportive changes occurring in the tumor microenvironment (TME) or tumor immune microenvironment (TIME) MICs, specifically emphasizing cGAS/STING signaling-dependent alteration. The article further discusses utilizing MIC-specific cGAS/STING signaling modulation as critical tumor immunotherapy to alter TIME.
Insights
Myeloid immune cells (MICs) detect cellular changes via pattern recognition receptors (PRRs). This review explores how cGAS/STING signaling in MICs impacts the tumor microenvironment (TME) and offers immunotherapy strategies.
Area of Science:
- Immunology
- Oncology
- Cellular Biology
Background:
- Myeloid immune cells (MICs) are crucial first responders to pathogens and cellular homeostasis disruptions.
- Cancer involves altered homeostasis, with MICs recognizing these changes through pattern recognition receptors (PRRs).
- Cytosolic PRRs, like cGAS/STING, detect double-stranded DNA (dsDNA), with longer dsDNA triggering stronger signaling.
Purpose of the Study:
- To discuss tumor-supportive alterations in MICs within the tumor microenvironment (TME).
- To emphasize the role of cGAS/STING signaling in modifying the tumor immune microenvironment (TIME).
- To explore the potential of modulating MIC-specific cGAS/STING signaling for cancer immunotherapy.
Main Methods:
- Review of existing literature on MICs, PRRs, and cGAS/STING signaling in cancer.
- Analysis of how cGAS/STING activation influences the TME.
- Discussion of therapeutic strategies targeting cGAS/STING in MICs.
Main Results:
- cGAS/STING signaling in MICs can promote tumor growth by altering the TME.
- The strength of cGAS/STING activation correlates with type 1 interferon and cytokine production.
- Dysregulation of cGAS/STING in MICs contributes to tumor progression.
Conclusions:
- Modulating MIC-specific cGAS/STING signaling is a promising avenue for cancer immunotherapy.
- Targeting cGAS/STING can reprogram the TIME to enhance anti-tumor immunity.
- Understanding cGAS/STING pathways in MICs is critical for developing novel cancer treatments.
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