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Acetate Decreases PVR/CD155 Expression via PI3K/AKT Pathway in Cancer Cells
Na Ly Tran1,2,# (Graduate Student), In Kyu Lee1,# (Post doc), Jung Kyun Choi1,2 (Graduate Student), Sang-Heon Kim1,2 (Professor), Seung Ja Oh 1,2,* (Senior Research Scientist)
1Center for Biomaterials, Biomedical Research Institute, Korea Institute of Science and Technology (KIST), Seoul, 02792, Republic of Korea,
2Division of Bio-Medical Science & Technology, Korea University of Science and Technology (UST), Daejeon 34113, Republic of Korea
In recent years, a growing interest has been garnered in the restoration of anti-tumor immunity in cancer treatment. As a potential therapeutic strategy, the benefits of immune checkpoint inhibitors have been demonstrated in many clinical studies. Although various methods have been applied to suppress immune checkpoints to boost anti-tumor immunity, including immune checkpoint inhibitors, there still exist unmet clinical needs to improve the response rate of cancer treatment. Here, we show that acetate suppresses the expression of a ligand for immune checkpoint, poliovirus receptor (PVR/CD155), in colon cancer cells. We demonstrated that acetate treatment in the cancer cells enhances effector responses of CD8+ T cells via reduced expression of PVR/CD155. We also found that acetate reduces the expression of PVR/CD155 through the PI3K/AKT pathway deactivation. Together, we demonstrated that acetate mediated the expression of PVR/CD155 in cancer cells that might potentiate the anti-tumor immunity in the cancer microenvironment. Our findings indicate that maintaining particular acetate concentrations could represent a complementary treatment strategy in current cancer treatment.
Abstract, Accepted Manuscript(in press) [Submitted on May 6, 2021, Accepted on July 5, 2021]
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