Evidence map›Paper›PMID 30066852›Full record

ArticleInternational journal of oncology2018

Upregulation of PD‑L1 expression by resveratrol and piceatannol in breast and colorectal cancer cells occurs via HDAC3/p300‑mediated NF‑κB signaling.

Justin Lucas, Tze-Chen Hsieh, H Dorota Halicka, Zbigniew Darzynkiewicz, Joseph M Wu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
6.6field-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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  5. CBP/p300, a promising therapeutic target for prostate cancer.Journal of translational medicine · 2025
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9 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Justin LucasDepartment of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.
Tze-Chen HsiehDepartment of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.
H Dorota HalickaBrander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, NY 10595, USA.
Zbigniew DarzynkiewiczBrander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, NY 10595, USA.
Joseph M WuDepartment of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.
New York Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death ligand 1 (PD‑L1) expressed in cancer cells interacting with its receptor programmed cell death 1 (PD‑1) expressed in immune cells represents a regulatory axis linked to the suppression and evasion of host immune functions. The blockade of PD‑1/PD‑L1 interaction using monoclonal antibodies has emerged as an effective therapy for several solid tumors; however, durable response has been observed in a subset of patients with PD‑L1-positive tumors. Thus, the understanding of the mechanisms responsible for the expression of PD‑L1 in tumor cells may help to improve the response to PD‑L1 blockade therapies. In this study, we investigated whether resveratrol, a grape-derived stilbenoid with immunoregulatory activity, modulates the expression of PD‑L1 in breast and colorectal cancer cells. The surface expression of PD‑L1 was determined by flow cytometry in cancer cells treated with resveratrol and/or piceatannol. Each stilbenoid alone induced PD‑L1 and when used in combination, elicited a synergistic upregulation of PD‑L1 in some cell lines. The induction of PD‑L1 by the combined use of stilbenoids was most pronounced in the Cal51 triple-negative breast cancer (TNBC) and SW620 colon cancer cells. The observed induction of PD‑L1 was transcriptionally mediated by nuclear factor (NF)-κB, as shown by NF‑κB reporter assays, the nuclear accumulation of the p65 subunit of NF‑κB, inhibition by the IKK inhibitor, BMS‑345541, and histone the modification inhibitors, resminostat, entinostat or anacardic acid. Combined treatment with resveratrol and piceatannol also decreased tumor cell survival as indicated by the upregulation of the DNA damaging marker, γH2AX, the cleavage of caspase 3, the downregulation of the survival markers, p38-MAPK/c‑Myc, and G1-to-S cell cycle arrest.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsB7-H1 AntigenCell Line, TumorCell SurvivalColonic NeoplasmsE1A-Associated p300 ProteinFemaleG1 Phase Cell Cycle CheckpointsHistone Deacetylase 3Histone DeacetylasesHumansNF-kappa BProgrammed Cell Death 1 ReceptorResveratrolSignal TransductionStilbenes3,3',4,5'-tetrahydroxystilbeneB7-H1 AntigenCD274 protein, humanE1A-Associated p300 ProteinEP300 protein, humanHistone Deacetylase 3Histone DeacetylasesNF-kappa BPDCD1 protein, humanProgrammed Cell Death 1 ReceptorResveratrolStilbenes

Identifiers

PMID30066852
PMCPMC6086626
OpenAlexW2886450957

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.