Evidence map›Paper›PMID 40490793›Full record

ArticleWorld journal of surgical oncology2025

PINK1 suppresses malignant phenotypes in esophageal squamous cell carcinoma.

Xiangyun Lu, Yuhui Pei, Hao Peng, Man Li, Jing Li, Yongkun Yao, Lianghai Wang

Abstract read
In one paragraph

Article in World journal of surgical oncology, 2025. 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. Article
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.

Xiangyun Lu *NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Yuhui Pei *NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Hao PengNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Man LiNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Jing LiNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Yongkun YaoNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, First Affiliated Hospital/School of Medicine, Shihezi University, Shihezi, Xinjiang, China. 284010875@qq.com.
Lianghai WangKey Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, Shihezi, Xinjiang, China. lh_wang@shzu.edu.cn.

Funding

Bingtuan Science and Technology Program 2022ZD002Science and Technology Program of Shihezi University RCZK202450Science and Technology Program of Shihezi University ZZZC202133
6 · The paper itself

Abstract

objectiveEsophageal squamous cell carcinoma (ESCC) is a common tumor characterized by a poor prognosis. PINK1 is strongly associated with tumorigenesis. However, the role of PINK1 in the progression of ESCC has not been elucidated.

methodsThe expression levels of PINK1 in tumor samples and corresponding normal tissues were evaluated using RNA-sequencing and gene expression array datasets. Pathway enrichment and immune infiltration analyses were performed to explore the role of PINK1 in ESCC development. Subsequently, cell counting kit-8, colony-forming assay, and Transwell assays were implemented to measure the proliferation and motility of ESCC cells. The glucose, ATP, pyruvate, and lactate concentrations were measured using suitable assay kits.

resultsPINK1 expression was significantly lower in ESCC samples across independent cohorts. In vitro assays demonstrated that PINK1 could inhibit the proliferation, migration, and invasive capabilities of ESCC cells. Furthermore, PINK1 could decrease intracellular glucose, lactic acid, pyruvic acid, and ATP levels in ESCC cells, whereas the glycolytic inhibitor 2-DG could abrogate its effect. Additionally, immunosuppressive-related gene sets were enriched in the PINK1 low-expression group. Immune infiltration analysis revealed that PINK1 expression was positively correlated with dendritic cells and T helper 1 cells within the tumor microenvironment.

conclusionsPINK1 inhibits cell growth, movement, glycolysis, and immune activation in ESCC, making it a promising therapeutic target.

Indexed as

Biomarkers, TumorEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaProtein KinasesCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMalePhenotypePrognosisPTEN-Induced Putative KinaseTumor Cells, CulturedBiomarkers, TumorProtein KinasesPTEN-Induced Putative KinaseESCCGlycolysisImmune activationMotilityPINK1Proliferation

Identifiers

PMID40490793
PMCPMC12147372

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.