Evidence map›Paper›PMID 29422611›Full record

ArticleOncogene2018

Decitibine improve the efficiency of anti-PD-1 therapy via activating the response to IFN/PD-L1 signal of lung cancer cells.

Qi Lai, Haiyong Wang, Angui Li, Yinhui Xu, Liang Tang, Qiang Chen, Chunfang Zhang, Yang Gao, Jianfei Song, Zhenzong Du

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. 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
3.3field-weighted citation impact, top 6% 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, 72 citations in OpenAlex.

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  6. The role of tumor-associated macrophages in tumor immune evasion.Journal of cancer research and clinical oncology · 2024
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  13. Targeting CXCL9/10/11-CXCR3 axis: an important component of tumor-promoting and antitumor immunity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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 1 country.

Qi LaiDepartment of Thoracic Surgery, Xiangya Hospital Cental South University, Changsha, Hunan, China.
Haiyong WangDepartment of Thoracic and Cardiovascular Surgery, The Affiliated Hospital of Guilin Medical University, Guilin, China.
Angui LiDepartment of Thoracic and Cardiovascular Surgery, The Affiliated Hospital of Guilin Medical University, Guilin, China.
Yinhui XuDepartment of Cardiothoracic Surgery, Affiliated Nanxi Shan Hospital of Guilin Medical University; Nanxi Shan Hospital of Guangxi Zhuang Autonomous Region, Guilin, Guangxi, China.
Liang TangDepartment of Cardiothoracic Surgery, Affiliated Nanxi Shan Hospital of Guilin Medical University; Nanxi Shan Hospital of Guangxi Zhuang Autonomous Region, Guilin, Guangxi, China.
Qiang ChenDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Chunfang ZhangDepartment of Thoracic Surgery, Xiangya Hospital Cental South University, Changsha, Hunan, China.
Yang GaoDepartment of Thoracic Surgery, Xiangya Hospital Cental South University, Changsha, Hunan, China.
Jianfei SongDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Guilin Medical University, Guilin, China. guilinsjf@163.com.
Zhenzong DuDepartment of Thoracic Surgery, Xiangya Hospital Cental South University, Changsha, Hunan, China. duzhenzong@sina.com.
Guilin Medical University · CNCentral South University · CNNanxi Mountain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IFN-γ-induced PD-L1 expression represents the existence of tumor-specific T cells, which predicts high-response rate to anti-PD-1/L1 therapy, but loss-of-function of IFN signals (e.g., JAK mutation) induces adaptive immune resistance in patients with low-response rate. Interferon regulatory factors (IRF) are frequently epigenetic silenced in carcinogenesis, while the role of methylation in anti-PD-1/L1 therapy remains unclear. We here investigated the methylation status of IFN-γ related genes IRF1/8 and IFN-α/β-related genes IRF3/7 in lung cancer tissues and found that only highly methylated IRF1 and 7 negatively correlated to cd274 (coding PD-L1) expression, similar to JAK mutation. Interestingly, decitibine (DAC) as methylation inhibitor could hypomethylate IRF1/7 to restore PD-L1 level. Meanwhile, IRF7 enhanced constitutive PD-L1 expression, which was independent of IFN-γ though directly promote transcription of PD-L1, leading to abrogating cytotoxic T lymphocytes (CTLs) generation which could be restored by anti-PD-L1 antibody, or siRNA-IRF7. The supplement of DAC to anti-PD-1 therapy in vivo improve the efficiency of anti-tumor with less methylated IRF1/7, more interferon-related genes expression (e.g., CXCL9) and IFN-γ/CD8+ T-cells infiltrations, suggesting that additional treatment of DAC could rescue the ability to response to IFN in lung cancer patients with anti-PD-1/L1 therapy resistance.

Indexed as

A549 CellsAdultAgedAged, 80 and overAnimalsAntibodies, MonoclonalAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, Lewis LungCell Line, TumorDecitabineDrug SynergismFemaleHEK293 CellsHumansInterferonsLung NeoplasmsAntibodies, MonoclonalDecitabineInterferonsPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID29422611
OpenAlexW2793835936

What OpenQuestion holds

Textmetadata
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.