Evidence map›Paper›PMID 42560586›Full record

ArticleMolecular biology reports2026

eIF6 affects the occurrence and development of esophageal cancer.

Cong-Gai Huang, Xin Zhou, Ran Huang, Hui-Ling Zhang, Chen-Xi Li, Fei Du, Hong Lei, Qiong Dai, Zhi-Hui Yang

Abstract read
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In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

9 authors.

Cong-Gai HuangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China.
Xin ZhouDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China.
Ran HuangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China.
Hui-Ling ZhangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China.
Chen-Xi LiDepartment of Oral and Maxillofacial Oncology and Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, 850042, People's Republic of China.
Fei DuDepartment of Pharmacy, The Fourth Affiliated Hospital of Southwest Medical University, Meishan, Sichuan, 646000, People's Republic of China.
Hong LeiDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China.
Qiong DaiDepartment of Human Anatomy, Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China. daiqiong@swmu.edu.cn.
Zhi-Hui YangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang, Luzhou, Sichuan, 646000, People's Republic of China. yzhih73@swmu.edu.cn.

Funding

Luzhou Science and Technology Program 2024JYJ061Sichuan Science and Technology Support Project 2022YFS0636Southwest Medical University research project 2024ZKZ005
6 · The paper itself

Abstract

objectiveEsophageal cancer (EC) ranks 11th in incidence and 7th in mortality among malignancies globally. The role of eukaryotic translation initiation factor 6 (eIF6) in esophageal squamous cell carcinoma (ESCA) progression, including its involvement in tumor development, invasion, and epithelial-mesenchymal transition (EMT), remains to be fully characterized.

methodsBioinformatic and immunohistochemistry (IHC) analyses of 114 ESCA cases demonstrated eIF6 upregulation, which was associated with lower tumor differentiation. Elevated eIF6 expression in ESCA cell lines (KYSE150, TE-1) relative to normal esophageal epithelial cells (HEEC) was verified by reverse transcription-quantitative PCR and western blotting. eIF6 silencing via short hairpin RNA (shRNA) attenuated ESCA cell proliferation, migration, and colony formation in vitro, as assessed by Cell Counting Kit-8, wound healing, and Transwell assays.

resultsBioinformatic analysis and IHC results showed that eIF6 protein was up-regulated in ESCC, and its expression level was inversely correlated with tumor differentiation degree. eIF6 knockdown was associated with reduced proliferation, migration, and colony formation of ESCC cells, accompanied by shifts in EMT markers, including increased E-cadherin and decreased N-cadherin and Vimentin levels. In addition, eIF6 depletion was accompanied by decreased phosphorylation of AKT (p-AKT

conclusionThese findings indicate an association between eIF6 upregulation and ESCA aggressiveness, along with concomitant changes in the PI3K/AKT/mTOR signaling pathway.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaPeptide Initiation FactorsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionEukaryotic Initiation FactorsFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesEIF6 protein, humanEukaryotic Initiation FactorsMTOR protein, humanPeptide Initiation FactorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesEMTEsophageal cancerEsophageal squamous cell carcinomaEukaryotic translation initiation factor 6PI3K/AKT/mTOR

Identifiers

PMID42560586

What Socratic holds

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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.