Evidence map›Paper›PMID 37185662›Full record

ArticleInternational journal of oral science2023

Down-regulation of DNA key protein-FEN1 inhibits OSCC growth by affecting immunosuppressive phenotypes via IFN-γ/JAK/STAT-1.

Shimeng Wang, Xiangjian Wang, Jun Sun, Jin Yang, Deyang Wu, Fanglong Wu, Hongmei Zhou

Open access · goldAbstract read
In one paragraph

Article in International journal of oral science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
9.7field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

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  18. When DNA-damage responses meet innate and adaptive immunity.Cellular and molecular life sciences : CMLS · 2024
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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

7 authors at 1 institution in 1 country.

Shimeng Wang *State Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Xiangjian Wang *State Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jun SunState Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jin YangState Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Deyang WuState Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Fanglong WuState Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China. wufanglong@scu.edu.cn.ORCID 0000-0003-4506-1387
Hongmei ZhouState Key Laboratory of Oral Diseases & National Center of Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, China. zhouhm@scu.edu.cn.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) escape from the immune system is mediated through several immunosuppressive phenotypes that are critical to the initiation and progression of tumors. As a hallmark of cancer, DNA damage repair is closely related to changes in the immunophenotypes of tumor cells. Although flap endonuclease-1 (FEN1), a pivotal DNA-related enzyme is involved in DNA base excision repair to maintain the stability of the cell genome, the correlation between FEN1 and tumor immunity has been unexplored. In the current study, by analyzing the clinicopathological characteristics of FEN1, we demonstrated that FEN1 overexpressed and that an inhibitory immune microenvironment was established in OSCC. In addition, we found that downregulating FEN1 inhibited the growth of OSCC tumors. In vitro studies provided evidence that FEN1 knockdown inhibited the biological behaviors of OSCC and caused DNA damage. Performing multiplex immunohistochemistry (mIHC), we directly observed that the acquisition of critical immunosuppressive phenotypes was correlated with the expression of FEN1. More importantly, FEN1 directly or indirectly regulated two typical immunosuppressive phenotype-related proteins human leukocyte antigen (HLA-DR) and programmed death receptor ligand 1 (PD-L1), through the interferon-gamma (IFN-γ)/janus kinase (JAK)/signal transducer and activator transcription 1 (STAT1) pathway. Our study highlights a new perspective on FEN1 action for the first time, providing theoretical evidence that it may be a potential immunotherapy target for OSCC.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMouth NeoplasmsDNADown-RegulationFlap EndonucleasesHumansInterferon-gammaJanus KinasesPhenotypeSquamous Cell Carcinoma of Head and NeckSTAT1 Transcription FactorTumor MicroenvironmentDNAFEN1 protein, humanFlap EndonucleasesIFNG protein, humanInterferon-gammaJanus KinasesSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID37185662
PMCPMC10130046
OpenAlexW4366990327

What OpenQuestion holds

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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.