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Article

The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells

by
Dong Young Kang
1,†,
Nipin Sp
1,†,
Eun Seong Jo
1,
Alexis Rugamba
1,
Dae Young Hong
2,
Hong Ghi Lee
3,
Ji-Seung Yoo
4,
Qing Liu
5,
Kyoung-Jin Jang
1,* and
Young Mok Yang
1,*
1
Department of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea
2
Department of Emergency Medicine, School of Medicine, Konkuk University, Seoul 05029, Korea
3
Division of Hematology-Oncology, Department of Internal Medicine, Konkuk University Medical Center, Seoul 05029, Korea
4
Department of Immunology, Hokkaido University Graduate School of Medicine, Sapporo 060-0808, Japan
5
Jilin Green Food Engineering Research Institute, Changchun 130000, Jilin, China
*
Authors to whom correspondence should be addressed.
†
These authors contribute equally to this paper.
Cancers 2020, 12(3), 727; https://doi.org/10.3390/cancers12030727
Submission received: 9 March 2020 / Revised: 16 March 2020 / Accepted: 16 March 2020 / Published: 19 March 2020
(This article belongs to the Special Issue Role of Natural Bioactive Compounds in the Rise and Fall of Cancers)
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Abstract

Non-small-cell lung cancer (NSCLC) is the most common lung cancer subtype and accounts for more than 80% of all lung cancer cases. Epidermal growth factor receptor (EGFR) phosphorylation by binding growth factors such as EGF activates downstream prooncogenic signaling pathways including KRAS-ERK, JAK-STAT, and PI3K-AKT. These pathways promote the tumor progression of NSCLC by inducing uncontrolled cell cycle, proliferation, migration, and programmed death-ligand 1 (PD-L1) expression. New cytotoxic drugs have facilitated considerable progress in NSCLC treatment, but side effects are still a significant cause of mortality. Gallic acid (3,4,5-trihydroxybenzoic acid; GA) is a phenolic natural compound, isolated from plant derivatives, that has been reported to show anticancer effects. We demonstrated the tumor-suppressive effect of GA, which induced the decrease of PD-L1 expression through binding to EGFR in NSCLC. This binding inhibited the phosphorylation of EGFR, subsequently inducing the inhibition of PI3K and AKT phosphorylation, which triggered the activation of p53. The p53-dependent upregulation of miR-34a induced PD-L1 downregulation. Further, we revealed the combination effect of GA and anti-PD-1 monoclonal antibody in an NSCLC-cell and peripheral blood mononuclear–cell coculture system. We propose a novel therapeutic application of GA for immunotherapy and chemotherapy in NSCLC.
Keywords: natural bioactive compound; gallic acid; EGFR signaling; p53; PD-L1; immunotherapy natural bioactive compound; gallic acid; EGFR signaling; p53; PD-L1; immunotherapy

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MDPI and ACS Style

Kang, D.Y.; Sp, N.; Jo, E.S.; Rugamba, A.; Hong, D.Y.; Lee, H.G.; Yoo, J.-S.; Liu, Q.; Jang, K.-J.; Yang, Y.M. The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells. Cancers 2020, 12, 727. https://doi.org/10.3390/cancers12030727

AMA Style

Kang DY, Sp N, Jo ES, Rugamba A, Hong DY, Lee HG, Yoo J-S, Liu Q, Jang K-J, Yang YM. The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells. Cancers. 2020; 12(3):727. https://doi.org/10.3390/cancers12030727

Chicago/Turabian Style

Kang, Dong Young, Nipin Sp, Eun Seong Jo, Alexis Rugamba, Dae Young Hong, Hong Ghi Lee, Ji-Seung Yoo, Qing Liu, Kyoung-Jin Jang, and Young Mok Yang. 2020. "The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells" Cancers 12, no. 3: 727. https://doi.org/10.3390/cancers12030727

APA Style

Kang, D. Y., Sp, N., Jo, E. S., Rugamba, A., Hong, D. Y., Lee, H. G., Yoo, J.-S., Liu, Q., Jang, K.-J., & Yang, Y. M. (2020). The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells. Cancers, 12(3), 727. https://doi.org/10.3390/cancers12030727

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