Evidence map›Paper›PMID 27329034›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Inhibition of SALL4 reduces tumorigenicity involving epithelial-mesenchymal transition via Wnt/β-catenin pathway in esophageal squamous cell carcinoma.

Jing He, Mingxia Zhou, Xinfeng Chen, Dongli Yue, Li Yang, Guohui Qin, Zhen Zhang, Qun Gao, Dan Wang, Chaoqi Zhang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% of its field
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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  20. Pluripotency Stemness and Cancer: More Questions than Answers.Advances in experimental medicine and biology · 2022
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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

15 authors at 3 institutions in 2 countries.

Jing HeBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Mingxia ZhouBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Xinfeng ChenBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Dongli YueBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Li YangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Guohui QinBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Zhen ZhangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Qun GaoBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Dan WangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Chaoqi ZhangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Lan HuangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Liping WangDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Bin ZhangDepartment of Hematology/Oncology, School of Medicine, Northwestern University, Chicago, IL60611, USA.
Jane YuDepartment of Internal Medicine, College of Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH, 45267, USA.
Yi ZhangBiotherapy Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China. yizhang@zzu.edu.cn.
First Affiliated Hospital of Zhengzhou University · CNNorthwestern University · USUniversity of Cincinnati Medical Center · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
NCI NIH HHS P30 CA060553
6 · The paper itself

Abstract

backgroundGrowing evidence suggests that SALL4 plays a vital role in tumor progression and metastasis. However, the molecular mechanism of SALL4 promoting esophageal squamous cell carcinoma (ESCC) remains to be elucidated.

methodsThe gene and protein expression profiles- were examined by using quantitative real-time PCR, immunohistochemistry and western blotting. Small hairpin RNA was used to evaluate the role of SALL4 both in cell lines and in animal models. Cell proliferation, apoptosis and invasion were assessed by CCK8, flow cytometry and transwell-matrigel assays. Sphere formation assay was used for cancer stem cell derivation and characterization.

resultsOur study showed that the transcription factor SALL4 was overexpressed in a majority of human ESCC tissues and closely correlated with a poor outcome. We established the lentiviral system using short hairpin RNA to knockdown SALL4 in TE7 and EC109 cells. Silencing of SALL4 inhibited the cell proliferation, induced apoptosis and the G1 phase arrest in cell cycle, decreased the ability of migration/invasion, clonogenicity and stemness in vitro. Besides, down-regulation of SALL4 enhanced the ESCC cells' sensitivity to cisplatin. Xenograft tumor models showed that silencing of SALL4 decreased the ability to form tumors in vivo. Furthermore, our study demonstrated that SALL4 played a vital role in modulating the stemness of ESCC cells via Wnt/β-catenin signaling pathway and in epithelial-mesenchymal transition.

conclusionsOur results revealed that SALL4 might serve as a functional marker for ESCC cancer stem cell, a crucial marker for prognosis and an attractive candidate for target therapy of ESCC.

Indexed as

Up-RegulationAnimalsApoptosisCarcinoma, Squamous CellCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleSALL4 protein, humanTranscription FactorsEpithelial-mesenchymal transition (EMT)Esophageal squamous cell carcinoma (ESCC)Prognostic markerSALL4Stemness

Identifiers

PMID27329034
PMCPMC4915037
OpenAlexW2471237755

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.