Evidence map›Paper›PMID 38291473›Full record

ArticleCell communication and signaling : CCS2024

Tumorous IRE1α facilitates CD8

Yuqi Yang, Sijia Wang, Xiang-Xu Wang, Sen Guo, Huina Wang, Qiong Shi, Yangzi Tian, Hao Wang, Tao Zhao, Hengxiang Zhang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
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  8. Review
  9. Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026
    Review
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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

15 authors at 3 institutions in 1 country.

Yuqi Yang *Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Sijia Wang *Department of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xiang-Xu Wang *Department of Clinical Oncology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Sen GuoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Huina WangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Qiong ShiDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Yangzi TianDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Hao WangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Tao ZhaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Hengxiang ZhangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Baolu ZhangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Tianwen GaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Chunying LiDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. lichying@fmmu.edu.cn.
Xiuli YiDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. yixiuli@fmmu.edu.cn.
Weinan GuoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. guown@fmmu.edu.cn.
Xijing Hospital · CNAir Force Medical University · CNSouthern Medical University · CN

Funding

National Natural Science Foundation of China 82273101National Natural Science Foundation of China 82273182Support Program of Young Talents in Shaanxi Province 20200303the key research and development of Shaanxi province 2022SF-178Young Eagle Project of Fourth Military Medical University 2019cyjhgwn
6 · The paper itself

Abstract

backgroundTumor cells frequently suffer from endoplasmic reticulum (ER) stress. Previous studies have extensively elucidated the role of tumorous unfolded protein response in melanoma cells, whereas the effect on tumor immunology and the underlying mechanism remain elusive.

methodsBioinformatics, biochemical assays and pre-clinical mice model were employed to demonstrate the role of tumorous inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) in anti-tumor immunity and the underlying mechanism.

resultsWe firstly found that IRE1α signaling activation was positively associated with the feature of tumor-infiltrating lymphocytes. Then, pharmacological ER stress induction by HA15 exerted prominent anti-tumor effect in immunocompetent mice and was highly dependent on CD8

conclusionsTumorous IRE1α facilitates CD8

Indexed as

MelanomaAnimalsCD8-Positive T-LymphocytesChemokinesCytokinesEndoribonucleasesMiceNF-kappa BProtein Serine-Threonine KinasesT-LymphocytesTumor MicroenvironmentChemokinesCytokinesEndoribonucleasesErn1 protein, mouseNF-kappa BProtein Serine-Threonine KinasesAnti-PD-1 antibodyER stressImmunosurveillanceImmunotherapyMelanoma

Identifiers

PMID38291473
PMCPMC10826282
OpenAlexW4391361499

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.