Wild Jujube suppresses growth of bronchial epithelial cells and upregulates PDL1 and OX40L
Location
E4110
Document Type
Poster
Start Date
30-11-2023 1:05 PM
End Date
30-11-2023 1:45 PM
Description
Abstract
Background: Lung cancer is the leading death-causing cancer in the US. Wild Jujube (WJ) is a popular fruit in Asia and has been shown to have anti-cancer properties including lung cancer. However, little is known about its effects on normal bronchial epithelial cells. Co-stimulatory molecules such as PDL1, PDL2, 4-1BBL, OX40L, and CD74 are a group of cell-surface molecules activating or inhibiting T cells. These molecules play a critical role in T-cell activation against cancer. However, the role of WJ on the expression of the co-stimulatory molecules is unknown yet. This study will investigate the effects of WJ on growth in bronchial epithelial cells and on the expression of key co-stimulatory molecules.
Methods: Normal bronchial epithelial cell line, B2B, was treated with WJ extract (WJE). Clonogenic Survival Assay and Cell Proliferation kit were utilized to measure the growth of B2B in the presence of WJE. RT-PCR and IHC were utilized to determine the effects of WJE extract on expression of key co-stimulatory molecules PDL1, PDL2, 4-1BBL, OX40L, and CD74.
Results: The percentage of colonies of B2B cells was significantly lower in the presence of WJE. In line with this, a decrease in the OD value of B2B cells in the presence of WJE was also found. PDL1, PDL2, 4-1BBL, OX40L and CD74 were constitutively expressed in B2B cells. The mRNA expression levels of PDL2, 4-1BBL, and CD74 were comparable in the presence of WJE to those in the absence of WJE. However, the mRNA expression levels of PDL1 and OX40L were much higher in the presence of WJE. IHC for PDL1 and OX40L is in progress.
Conclusion: WJ suppresses the growth of bronchial epithelial cells and upregulates the expression of PDL1 and OX40L. The clinical significance of the upregulation of OX40L is unclear. However, the upregulation of PDL1 by WJ may protect normal bronchial epithelial cells from immune attack while lung cancer cells are targeted by immunity. Such a study may provide useful information to design WJ as an option for the treatment of lung cancer.
Recommended Citation
Shrivastava, Rhea; Zhao, Lei; Cowan, Braydon; Mayberry, Trent; Heines, Nathan; Krenn, Weston; Wakefield, Mark R.; Wang, Yongsheng; and Fang, Yujiang, "Wild Jujube suppresses growth of bronchial epithelial cells and upregulates PDL1 and OX40L" (2023). DMU Research Symposium. 30.
https://digitalcommons.dmu.edu/researchsymposium/2023rs/2023abstracts/30
Wild Jujube suppresses growth of bronchial epithelial cells and upregulates PDL1 and OX40L
E4110
Abstract
Background: Lung cancer is the leading death-causing cancer in the US. Wild Jujube (WJ) is a popular fruit in Asia and has been shown to have anti-cancer properties including lung cancer. However, little is known about its effects on normal bronchial epithelial cells. Co-stimulatory molecules such as PDL1, PDL2, 4-1BBL, OX40L, and CD74 are a group of cell-surface molecules activating or inhibiting T cells. These molecules play a critical role in T-cell activation against cancer. However, the role of WJ on the expression of the co-stimulatory molecules is unknown yet. This study will investigate the effects of WJ on growth in bronchial epithelial cells and on the expression of key co-stimulatory molecules.
Methods: Normal bronchial epithelial cell line, B2B, was treated with WJ extract (WJE). Clonogenic Survival Assay and Cell Proliferation kit were utilized to measure the growth of B2B in the presence of WJE. RT-PCR and IHC were utilized to determine the effects of WJE extract on expression of key co-stimulatory molecules PDL1, PDL2, 4-1BBL, OX40L, and CD74.
Results: The percentage of colonies of B2B cells was significantly lower in the presence of WJE. In line with this, a decrease in the OD value of B2B cells in the presence of WJE was also found. PDL1, PDL2, 4-1BBL, OX40L and CD74 were constitutively expressed in B2B cells. The mRNA expression levels of PDL2, 4-1BBL, and CD74 were comparable in the presence of WJE to those in the absence of WJE. However, the mRNA expression levels of PDL1 and OX40L were much higher in the presence of WJE. IHC for PDL1 and OX40L is in progress.
Conclusion: WJ suppresses the growth of bronchial epithelial cells and upregulates the expression of PDL1 and OX40L. The clinical significance of the upregulation of OX40L is unclear. However, the upregulation of PDL1 by WJ may protect normal bronchial epithelial cells from immune attack while lung cancer cells are targeted by immunity. Such a study may provide useful information to design WJ as an option for the treatment of lung cancer.
