Evidence map›Paper›PMID 36357569›Full record

ArticleExperimental & molecular medicine2022

WNK3 inhibition elicits antitumor immunity by suppressing PD-L1 expression on tumor cells and activating T-cell function.

Hyun Ju Yoon, Gi-Cheon Kim, Sejin Oh, Hakhyun Kim, Yong Keon Kim, Yunji Lee, Min Seo Kim, Gino Kwon, Yeon-Su Ok, Ho-Keun Kwon and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. A Phase II Multicenter Trial of Rucaparib and Nivolumab as Maintenance Therapy in Patients with Advanced Biliary Tract Cancer: BilT-02.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

11 authors at 1 institution in 1 country.

Hyun Ju Yoon *Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Gi-Cheon Kim *Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, Korea.
Sejin OhSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Hakhyun KimGraduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Korea.
Yong Keon KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Yunji LeeSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Min Seo KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Gino KwonGraduate Program for Nanomedical Science, Yonsei University, Seoul, Korea.
Yeon-Su OkGraduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Korea.
Ho-Keun KwonGraduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Korea. hk@yuhs.ac.
Hyun Seok KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea. hsfkim@yuhs.ac.ORCID 0000-0003-4498-8690
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint therapies, such as programmed cell death ligand 1 (PD-L1) blockade, have shown remarkable clinical benefit in many cancers by restoring the function of exhausted T cells. Hence, the identification of novel PD-L1 regulators and the development of their inhibition strategies have significant therapeutic advantages. Here, we conducted pooled shRNA screening to identify regulators of membrane PD-L1 levels in lung cancer cells targeting druggable genes and cancer drivers. We identified WNK lysine deficient protein kinase 3 (WNK3) as a novel positive regulator of PD-L1 expression. The kinase-dead WNK3 mutant failed to elevate PD-L1 levels, indicating the involvement of its kinase domain in this function. WNK3 perturbation increased cancer cell death in cancer cell-immune cell coculture conditions and boosted the secretion of cytokines and cytolytic enzymes, promoting antitumor activities in CD4

Indexed as

B7-H1 AntigenCD8-Positive T-LymphocytesLung NeoplasmsProtein Serine-Threonine KinasesAnimalsCell Line, TumorHumansImmunotherapyMiceB7-H1 AntigenProtein Serine-Threonine KinasesWNK3 protein, human

Identifiers

PMID36357569
PMCPMC9722663
OpenAlexW4308891229

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.