Evidence map›Paper›PMID 36109513›Full record

ArticleCell death & disease2022

STING mediates nuclear PD-L1 targeting-induced senescence in cancer cells.

Je-Jung Lee, So Young Kim, Songhee H Kim, Seoyeon Choi, Bin Lee, Jeon-Soo Shin

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  7. Analysis of PD-L1 Transcriptional Activity by Chromatin Immunoprecipitation.Methods in molecular biology (Clifton, N.J.) · 2026
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  13. NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

6 authors at 1 institution in 1 country.

Je-Jung Lee *Department of Microbiology, Yonsei University College of Medicine, Seoul, South Korea.
So Young Kim *Department of Microbiology, Yonsei University College of Medicine, Seoul, South Korea.
Songhee H KimInstitute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, South Korea.
Seoyeon ChoiDepartment of Microbiology, Yonsei University College of Medicine, Seoul, South Korea.
Bin LeeDepartment of Microbiology, Yonsei University College of Medicine, Seoul, South Korea.
Jeon-Soo ShinDepartment of Microbiology, Yonsei University College of Medicine, Seoul, South Korea. jsshin6203@yuhs.ac.ORCID 0000-0002-8294-3234
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint molecule programmed death-ligand 1 (PD-L1) is overexpressed in cancer cells and imparts resistance to cancer therapy. Although membrane PD-L1 has been targeted for cancer immune therapy, nuclear PD-L1 was reported to confer cancer resistance. Therefore, it is important to regulate the nuclear PD-L1. The mechanisms underlying the therapeutic efficacy of PD-L1 targeting have not been well-established. Cellular senescence has been considered a pivotal mechanism to prevent cancer progression, and recently, PD-L1 inhibition was shown to be involved in cancer cell senescence. However, the relevance of PD-L1 targeting-induced senescence and the role of stimulator of interferon genes (STING) has not been reported. Therefore, we aimed to identify the role of PD-L1 in cancer progression and how it regulates cancer prevention. In this study, we found that PD-L1 depletion-induced senescence via strong induction of STING expression in mouse melanoma B16-F10 and colon cancer CT26 cells, and in human melanoma A375 and lung cancer A549 cells. Interestingly, nuclear PD-L1 silencing increased STING promoter activity, implying that PD-L1 negatively regulates STING expression via transcriptional modulation. Furthermore, we showed that PD-L1 binds to the STING promoter region, indicating that PD-L1 directly controls STING expression to promote cancer growth. In addition, when we combined PD-L1 silencing with the senescence-inducing chemotherapeutic agent doxorubicin, the effect of PD-L1-targeting was even more powerful. Overall, our findings can contribute to the understanding of the role of PD-L1 in cancer therapy by elucidating a novel mechanism for PD-L1 targeting in cancer cells.

Indexed as

B7-H1 AntigenMelanomaAnimalsDoxorubicinHumansImmune Checkpoint ProteinsInterferonsMembrane ProteinsMiceSTING ProteinB7-H1 AntigenCD274 protein, humanDoxorubicinImmune Checkpoint ProteinsInterferonsMembrane ProteinsSTING1 protein, humanSting1 protein, mouseSTING Protein

Identifiers

PMID36109513
PMCPMC9477807
OpenAlexW4295925138

What OpenQuestion holds

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LicenceCC BY
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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.