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Acetate decreases PVR/CD155 expression via PI3K/AKT pathway in cancer cells
Na Ly Tran1, In Kyu Lee2, Jungkyun Choi1
1Center for Biomaterials, Biomedical Research Institute, Korea Institute of Science and Technology (KIST), Seoul 02792; Division of Bio-Medical Science & Technology, KIST school, Korea University of Science and Technology (UST), Daejeon 02792, Korea.
Abstract:
In recent years, restoring anti-tumor immunity has garnered a growing interest in cancer treatment. As potential therapeutics, immune checkpoint inhibitors have demonstrated benefits in many clinical studies. Although various methods have been applied to suppress immune checkpoints to boost anti-tumor immunity, including the use of immune checkpoint inhibitors, there are still unmet clinical needs to improve the response rate of cancer treatment. Here, we show that acetate can suppress the expression of poliovirus receptor (PVR/CD155), a ligand for immune checkpoint, in colon cancer cells. We demonstrated that acetate treatment could enhance effector responses of CD8+ T cells by decreasing the expression of PVR/CD155 in cancer cells. We also found that acetate could reduce the expression of PVR/CD155 by deactivating the PI3K/AKT pathway. These results demonstrate that acetate-mediated expression of PVR/ CD155 in cancer cells might potentiate the anti-tumor immunity in the microenvironment of cancer. Our findings indicate that maintaining particular acetate concentrations could be a complementary strategy in current cancer treatment. [BMB Reports 2021; 54(8): 431-436].
Insights
Acetate suppresses immune checkpoint ligand PVR/CD155 in colon cancer cells, enhancing CD8+ T cell responses. This finding suggests acetate as a potential complementary strategy to boost anti-tumor immunity in cancer treatment.
Area of Science:
- Immunology
- Oncology
- Metabolism
Background:
- Restoring anti-tumor immunity is crucial for effective cancer treatment.
- Immune checkpoint inhibitors show promise but have limitations, highlighting the need for novel therapeutic strategies.
- Poliovirus receptor (PVR/CD155), a ligand for immune checkpoints, is implicated in tumor immune evasion.
Purpose of the Study:
- To investigate the effect of acetate on the expression of poliovirus receptor (PVR/CD155) in colon cancer cells.
- To determine if acetate can modulate anti-tumor immunity by affecting PVR/CD155 expression.
- To explore the molecular mechanisms underlying acetate's action on PVR/CD155.
Main Methods:
- Treatment of colon cancer cells with acetate.
- Assessment of PVR/CD155 expression levels.
- Evaluation of CD8+ T cell effector responses.
- Analysis of the PI3K/AKT signaling pathway.
Main Results:
- Acetate significantly suppressed PVR/CD155 expression in colon cancer cells.
- Acetate treatment enhanced CD8+ T cell effector responses by reducing PVR/CD155 on cancer cells.
- Acetate deactivated the PI3K/AKT pathway, leading to decreased PVR/CD155 expression.
Conclusions:
- Acetate can potentiate anti-tumor immunity by downregulating PVR/CD155 expression in cancer cells.
- Acetate's mechanism involves the deactivation of the PI3K/AKT pathway.
- Maintaining specific acetate concentrations may serve as an adjunctive approach in cancer therapy to enhance immune responses.
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