Evidence map›Paper›PMID 32204508›Full record

ArticleCancers2020

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

Dong Young Kang, Nipin Sp, Eun Seong Jo, Alexis Rugamba, Dae Young Hong, Hong Ghi Lee, Ji-Seung Yoo, Qing Liu, Kyoung-Jin Jang, Young Mok Yang

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 82 citations in OpenAlex.

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  18. How gallic acid regulates molecular signaling: role in cancer drug resistance.Medical oncology (Northwood, London, England) · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Dong Young KangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Nipin SpDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Eun Seong JoDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Alexis RugambaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Dae Young HongDepartment of Emergency Medicine, School of Medicine, Konkuk University, Seoul 05029, Korea.
Hong Ghi LeeDivision of Hematology-Oncology, Department of Internal Medicine, Konkuk University Medical Center, Seoul 05029, Korea.
Ji-Seung YooDepartment of Immunology, Hokkaido University Graduate School of Medicine, Sapporo 060-0808, Japan.
Qing LiuJilin Green Food Engineering Research Institute, Changchun 130000, Jilin, China.
Kyoung-Jin JangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Young Mok YangDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Konkuk University · KRHokkaido University · JPKonkuk University Medical Center · KR

Funding

National Research Foundation of Korea 2018R1C1B6006146National Research Foundation of Korea 2019R1I1A1A01060399National Research Foundation of Korea 2019R1I1A1A01060537
6 · The paper itself

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.

Indexed as

EGFR signalinggallic acidimmunotherapynatural bioactive compoundp53PD-L1

Identifiers

PMID32204508
PMCPMC7140102
OpenAlexW3011396560

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.