Evidence map›Paper›PMID 42149295›Full record

ArticleApoptosis : an international journal on programmed cell death2026

PSD3 links autophagic flux to MHC-I-associated immune modulation in esophageal squamous cell carcinoma.

Shujuan Luo, Aididar Nurbahati, Bangwu Cai, Hong Cui, Tianyuan Peng, Wei Wang, Huifang Li, Jiao Chen, Qing Liu, Xiaomei Lu and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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.

Shujuan LuoState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Aididar NurbahatiState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Bangwu CaiState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Hong CuiState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Tianyuan PengState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Wei WangDepartment of Digestive Internal Medicine, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, 830011, People's Republic of China.
Huifang LiDepartment of Breast Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, People's Republic of China.
Jiao ChenState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Qing LiuState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China.
Xiaomei LuState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China. luxiaomei@xjmu.edu.cn.
Shutao ZhengState Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang Uygur Autonomous Region, People's Republic of China. zhengshutao@xjmu.edu.cn.

Funding

Key Project of Xinjiang Uygur Autonomous Region Natural Science Foundation 2022D01D69Leading Talent Project of Scientific and Technological Innovation in Tianshan Talents Training Plan of Xinjiang Uygur Autonomous Region 2022TSYCLJ0031Major Scientific Research Plan Cultivation Project of Xinjiang Medical University No.XYD2024ZX02Nature Science Foundation of China 82360521, 82260568State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia Fund SKL-HIDCA-2024-SG3Tianshan Talent Cultivation Plan for Young Top Talents Project of Xinjiang Uygur Autonomous Region 2024TSYCCX0103
6 · The paper itself

Abstract

Esophageal squamous cell carcinoma (ESCC) is characterized by immune evasion and poor clinical outcomes. Autophagy has been implicated in tumor-immune interactions, but the molecular factors linking autophagy-associated processes to immune modulation in ESCC remain incompletely defined. We analyzed PSD3 expression in ESCC tissues and its association with prognosis and MHC-I-related molecules. Protein interactions were assessed by co-immunoprecipitation. Autophagy-associated marker changes, autophagic flux, total MHC-I protein levels, and immune cell infiltration were evaluated following PSD3 knockdown in murine and human ESCC models using Western blotting, tandem fluorescent LC3 reporter assays, immunohistochemistry, and single-cell RNA sequencing. Epistasis analysis was performed by silencing ATG7 following PSD3 knockdown. PSD3 was upregulated in ESCC and associated with unfavorable prognosis. PSD3 knockdown was accompanied by changes in autophagy-associated markers and reduced autophagosome abundance. In KYSE150 cells, tandem fluorescent mCherry-eGFP-LC3B analysis showed that PSD3 silencing impaired autophagic flux. PSD3 co-immunoprecipitated with ATG7, BAG3 and TBK1, supporting its association with autophagy-related protein complexes. PSD3 knockdown increased total MHC-I protein levels and was associated with enhanced immune cell infiltration in syngeneic tumor models. Furthermore, ATG7 silencing following PSD3 knockdown selectively restored HLA-E expression, while HLA-ABC and HLA-F showed no clearly distinguishable change. These findings support a working model in which PSD3 is linked to autophagy-associated immune modulation in ESCC. While additional studies are required to define pathway hierarchy and antigen-presentation function more directly, PSD3 emerges as a candidate molecular node for further mechanistic and translational investigation.

Indexed as

AutophagyEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHistocompatibility Antigens Class IAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsAutophagy-Related Protein 7Cell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMicePrognosisProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsATG7 protein, humanAutophagy-Related Protein 7Histocompatibility Antigens Class IProtein Serine-Threonine KinasesTBK1 protein, humanAutophagyESCCImmune escapeMHC-IPSD3Tumor microenvironment

Identifiers

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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.