Evidence map›Paper›PMID 40235872›Full record

ArticleWorld journal of gastrointestinal oncology2025

Nitric oxide synthase 1 inhibits the progression of esophageal cancer through interacting with nitric oxide synthase 1 adaptor protein.

Zi-Wei Xiao, Ying-Chao Zeng, Lin-Tao Ji, Jia-Tao Yuan, Lin Li

Abstract read
In one paragraph

Article in World journal of gastrointestinal 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

5 authors.

Zi-Wei XiaoCollege of Medical, Hunan Normal University, Changsha 410081, Hunan Province, China.
Ying-Chao ZengCollege of Medical, Hunan Normal University, Changsha 410081, Hunan Province, China.
Lin-Tao JiCollege of Medical, Hunan Normal University, Changsha 410081, Hunan Province, China.
Jia-Tao YuanCollege of Medical, Hunan Normal University, Changsha 410081, Hunan Province, China.
Lin LiCollege of Medical, Hunan Normal University, Changsha 410081, Hunan Province, China. 18529482372@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal cancer (ESCA) is among the most prevalent and lethal tumors globally. While nitric oxide synthase 1 (NOS1) is recognized for its important involvement in various cancers, its specific function in ESCA remains unclear.

aimTo explore the potential role and underlying mechanisms of NOS1 in ESCA.

methodsSurvival rates were analyzed using GeneCards and Gene Expression Profiling Interactive Analysis. The effects and mechanisms of NOS1 on ESCA cells were evaluated

resultsThe survival rate of patients with ESCA with high NOS1 expression was higher than that of patients with low NOS1 expression. NOS1 expression in ESCA cell lines was lower than that in normal esophageal epithelial cells. Overexpression of NOS1 (oe-NOS1) inhibited proliferation, invasion, and migration abilities in ESCA cell lines, resulting in decreased autophagy levels and increased apoptosis, pyroptosis, and ferroptosis. Protein interaction studies confirmed the interaction between NOS1 and NOS1 adaptor protein (NOS1AP). Following oe-NOS1 and the silencing of NOS1AP, levels of P62 and microtubule-associated protein 1 light chain 3 beta increased both

conclusionNOS1 and NOS1 proteins interact to suppress autophagy, activate the PI3K/AKT pathway, and exert anti-cancer effects in ESCA.

Indexed as

AutophagyEsophageal cancerNitric oxide synthase 1Nitric oxide synthase 1 adaptor proteinPhosphatidylinositol 3-kinase/protein kinase B pathway

Identifiers

PMID40235872
PMCPMC11995332

What Socratic holds

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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 Socratic graph.