Evidence map›Paper›PMID 40856423›Full record

ArticleCancer medicine2025

The GNL3L-MDM2 Interaction Drives Esophageal Squamous Cell Carcinoma Progression.

Aijie Yang, Haiyun Song, Yufeng Cheng

Abstract read
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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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

3 authors.

Aijie YangDepartment of Radiotherapy, Qilu Hospital of Shandong University (Qingdao), Qingdao, China.
Haiyun SongDepartment of Pathology, Qilu Hospital of Shandong University (Qingdao), Qingdao, China.
Yufeng ChengDepartment of Radiation Oncology, Qilu Hospital of Shandong University, Jinan, China.ORCID https://orcid.org/0009-0001-6010-6822

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study investigates the mechanisms by which GNL3L influences ESCC progression.

methodsGNL3L expression was analyzed via immunohistochemistry in ESCC tissues. Cell proliferation (EdU and CCK8 assays), migration, invasion (wound healing and Transwell assays), cell cycle, and apoptosis (flow cytometry) were assessed. Levels of GNL3L, MDM2, p53, and p21 were evaluated by qRT-PCR and western blot. Tumor growth was observed in nude mice injected with TE-1 cells.

resultsGNL3L was upregulated in ESCC specimens (p < 0.05) and knockdown reduced proliferation and migration while enhancing apoptosis (p < 0.01). GNL3L interacted with MDM2; knocking down GNL3L decreased MDM2 and increased p53 and p21 (p < 0.01). MDM2 overexpression enhanced malignant characteristics, reversible by GNL3L silencing (p < 0.01). Moreover, MDM2 knockdown inhibited malignant characteristics, reversible by GNL3L overexpression (p < 0.01). In vivo, the sh-GNL3L group exhibited the smallest tumor volumes after 5 weeks (p < 0.01).

conclusionsGNL3L correlates with ESCC malignancy, influencing the MDM2-p53-p21 axis. GNL3L-MDM2 interaction is critical in ESCC progression.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaProto-Oncogene Proteins c-mdm2AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeCyclin-Dependent Kinase Inhibitor p21MDM2 protein, humanProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53apoptosisesophageal squamous cell carcinomaGNL3LinvasionMDM2proliferation

Identifiers

PMID40856423
PMCPMC12378702

What Socratic holds

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LicenceCC BY
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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.