Evidence map›Paper›PMID 29636641›Full record

ArticleCancer cell international2018

Down-regulation of STAT3 induces the apoptosis and G1 cell cycle arrest in esophageal carcinoma ECA109 cells.

Chao Zhou, Jie Ma, Mengyuan Su, Dan Shao, Jianan Zhao, Tongjian Zhao, Zhuoyao Song, Yan Meng, Ping Jiao

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Chao Zhou1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Jie Ma1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Mengyuan Su1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Dan Shao2The First Hospital of Jilin University, 1163 Xinmin Street, Changchun, Jilin 130021 People's Republic of China.
Jianan Zhao1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Tongjian Zhao1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Zhuoyao Song1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Yan Meng1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Ping Jiao1School of Pharmaceutical Sciences, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021 People's Republic of China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignal transducer and activator of transcription 3 (STAT3) is persistently activated in a wide variety of epithelial cancers. Aberrant activity of STAT3 correlates with tumor growth, invasion and metastasis, which makes it a potential therapeutic target of cancer. To explore the biological role of STAT3 in esophageal cancer, we used small hairpin RNA to knockdown the expression of the STAT3 gene in the esophageal carcinoma ECA109 cell line and the cell apoptosis, cell cycle and cell migration were investigated.

methodsThe cell apoptosis was tested using DNA ladder, mitochondrial membrane potential assay, TUNEL assay, annexin V-PI staining. Cell cycle phases were estimated using flow cytometry analysis. The mRNA and proteins related to apoptosis and cell cycle were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. And cell migration was investigated by in vitro Transwell assay. The data were analyzed with two-sample Student's t test and ANOVA followed by the LSD post hoc test.

resultsOur results showed that knockdown of STAT3 in ECA109 cells induced noticeable apoptotic morphological changes like cell shrinkage, apoptotic vacuoles, membrane blebbing time-dependently. In addition, DNA ladder, TUNEL assay, Annexin V-PI staining and declined level of cleaved Caspase-3 indicated that down-regulation of STAT3 could induce apoptosis in ECA109 cells. Flow cytometry analysis displayed the induction of G1-phase cell cycle arrest of ECA109 cells by STAT3 decreasing, consistent with the descend of c-Myc and cyclin D1 in protein levels. Furthermore, STAT3 knockdown suppressed the expression of matrix metalloproteinases-9, sushi domain containing 2 and urokinase plasminogen activator in ECA109 cells and inhibited cell migration ability.

conclusionsKnockdown of STAT3 could induce the apoptosis and G1 cell cycle arrest in esophageal carcinoma ECA109 cells, and inhibit the migration ability of cells as well.

Indexed as

ApoptosisEsophageal cancershRNASTAT3

Identifiers

PMID29636641
PMCPMC5883295
OpenAlexW2807088581

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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 OpenQuestion graph.