This study investigates the synergistic inhibitory effects of combining the stimulator of interferon genes (STING) agonist cyclic diadenylate monophosphate (c-di-AMP) and ginsenoside RG3 on cisplatin (DDP)-resistant gastric cancer (GC) cells. The objective is to identify novel therapeutic targets and offers insights for the clinical management of DDP resistance. Various techniques were employed, including western blot, MTT assay, colony formation assay, scratch assay, transwell assay, tubule formation assay, flow cytometry, Hoechst 33342 fluorescence staining, and in vivo experiments, to investigate the potential mechanisms and effects of the combined application of the STING agonist and ginsenoside RG3 in reversing cisplatin resistance in gastric cancer. The combination markedly suppressed key malignant behaviors, including proliferation, migration, invasion, and angiogenesis of SGC-7901/DDP cells. Additionally, this treatment inhibited the epithelial-mesenchymal transition (EMT) process and stem cell-like characteristics of SGC-7901/DDP cells, while downregulating the expression of resistance-related proteins. The STING agonist effectively suppresses the growth and proliferation of gastric cancer cells. Ginsenoside RG3, well-documented for its multifaceted properties, including antioxidant, anti-aging, and anti-cancer effects, is widely used in cancer treatment and in managing chemotherapy-related side effects. Furthermore, RG3 enhances anti-tumor immunity by regulating signal transduction. This study comprehensively evaluated the efficacy of the STING agonist and RG3 combination through in vitro and in vivo experiments, demonstrating significant inhibition of malignant progression and reversal of drug resistance in gastric cancer. These findings offer a robust theoretical foundation for clinical applications and highlight new therapeutic targets for future research.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745231PMC
http://dx.doi.org/10.1002/fsn3.4744DOI Listing

Publication Analysis

Top Keywords

sting agonist
20
gastric cancer
20
ginsenoside rg3
16
resistance gastric
12
cisplatin resistance
8
cancer cells
8
therapeutic targets
8
formation assay
8
in vivo experiments
8
sgc-7901/ddp cells
8

Similar Publications

Cytotoxic DNAs, methylation, histones and histones binding proteins are speculated to induce DNA sensors. Under stressed condition, the antigenic patterns, PAMPs and DAMPs, trigger the hyperactive innate response through DNA, DNA-RNA hybrids, oligonucleotides, histones and mtDNA to initiate cGAMP-STING-IFN I cascade. HSV -1&2, HIV, Varicella- Zoster virus, Polyomavirus, Cytomegalovirus, and KSHV negatively regulate the STING-MAVS-TBK-1/1KKE pathway.

View Article and Find Full Text PDF

Diabetic vascular aging is driven by macrophage senescence, which propagates senescence-associated secretory phenotypes (SASP), exacerbating vascular dysfunction. This study utilized a type 2 diabetes mellitus (T2DM) mouse model induced by streptozotocin injection and a high-fat diet to investigate the role of STING in macrophage senescence. Vascular aging markers and senescent macrophages were assessed , while , high glucose treatment induced macrophage senescence, enhancing senescence in co-cultured vascular smooth muscle cells.

View Article and Find Full Text PDF

This study investigates the synergistic inhibitory effects of combining the stimulator of interferon genes (STING) agonist cyclic diadenylate monophosphate (c-di-AMP) and ginsenoside RG3 on cisplatin (DDP)-resistant gastric cancer (GC) cells. The objective is to identify novel therapeutic targets and offers insights for the clinical management of DDP resistance. Various techniques were employed, including western blot, MTT assay, colony formation assay, scratch assay, transwell assay, tubule formation assay, flow cytometry, Hoechst 33342 fluorescence staining, and in vivo experiments, to investigate the potential mechanisms and effects of the combined application of the STING agonist and ginsenoside RG3 in reversing cisplatin resistance in gastric cancer.

View Article and Find Full Text PDF

STING in Cancer Immunoediting: Modeling Tumor-Immune Dynamics Throughout Cancer Development.

Cancer Lett

January 2025

Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, People's Republic of China; Department of Pathology, Harbin Medical University, Harbin, 150081, China. Electronic address:

Cancer immunoediting is a dynamic process of tumor-immune system interaction that plays a critical role in cancer development and progression. Recent studies have highlighted the importance of innate signaling pathways possessed by both cancer cells and immune cells in this process. The STING molecule, a pivotal innate immune signaling molecule, mediates DNA-triggered immune responses in both cancer cells and immune cells, modulating the anti-tumor immune response and shaping the efficacy of immunotherapy.

View Article and Find Full Text PDF

Objective: Cell dysfunction and death induced by lung ischaemia-reperfusion injury (LIRI) are the main causes of death in transplant patients. Activation of the cGAS-STING-induced immune response and death plays a critical role in multiple organ injuries. However, no study has yet investigated the role of the cGAS-STING pathway in LIRI after lung transplantation.

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!