Evidence map›Paper›PMID 34128372›Full record

ArticleJournal of Zhejiang University. Science. B2021

Blocking the JAK2/STAT3 and ERK pathways suppresses the proliferation of gastrointestinal cancers by inducing apoptosis.

Xi Wang, Chunyan Dai, Yifei Yin, Lin Wu, Weiyang Jin, Yufei Fu, Zhe Chen, Ke Hao, Bin Lu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 21 citations in OpenAlex.

  1. Targetable pathways for drug repurposing in gastric cancer.World journal of gastroenterology · 2025
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  4. Natural products targeting the MAPK-signaling pathway in cancer: overview.Journal of cancer research and clinical oncology · 2024
    Review
  5. Review
  6. Article
  7. 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

9 authors at 3 institutions in 1 country.

Xi WangKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Chunyan DaiKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Yifei YinKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Lin WuCollege of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Weiyang JinCollege of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou 310036, China.
Yufei FuKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Zhe ChenKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Ke HaoResearch Center of Blood Transfusion Medicine, Ministry of Education Key Laboratory of Laboratory Medicine, Department of Blood Transfusion, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, China.
Bin LuKey Laboratory of Digestive Pathophysiology of Zhejiang Province, the First Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang Chinese Medical University, Hangzhou 310006, China.
Zhejiang Chinese Medical University · CNHangzhou Normal University · CNBlood Center of Zhejiang Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated crosstalk between different signaling pathways contributes to tumor development, including resistance to cancer therapy. In the present study, we found that the mitogen-activated extracellular signal-regulated kinase (MEK) inhibitor trametinib failed to suppress the proliferation of PANC-1 and MGC803 cells by activating the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, while the JAK2 inhibitor fedratinib failed to inhibit the growth of the PANC-1 cells upon stimulation of extracellular signal-regulated kinase (ERK) signaling. In particular, the most prominent enhancement of the anti-proliferative effect resulted from the concurrent blockage of the JAK2/STAT3 and ERK signaling pathways. Furthermore, the combination of the two inhibitors resulted in a reduced tumor burden in mice. Our evidence suggests novel crosstalk between JAK2/STAT3 and ERK signaling in gastric cancer (GC) and pancreatic ductal adenocarcinoma (PDAC) cells and provides a therapeutic strategy to overcome potential resistance in gastrointestinal cancer.

Indexed as

AnimalsApoptosisBenzenesulfonamidesCell Line, TumorCell ProliferationExtracellular Signal-Regulated MAP KinasesFemaleGastrointestinal NeoplasmsHumansJanus Kinase 2MiceMice, Inbred BALB CProtein Kinase InhibitorsPyridonesPyrimidinonesPyrrolidinesBenzenesulfonamidesExtracellular Signal-Regulated MAP KinasesfedratinibJAK2 protein, humanJanus Kinase 2Protein Kinase InhibitorsPyridonesPyrimidinonesPyrrolidinesStat3 protein, mouseSTAT3 Transcription FactorSulfonamidestrametinibApoptosisCrosstalkERK pathwayGastrointestinal cancersJAK2/STAT3 pathway

Identifiers

PMID34128372
PMCPMC8214945
OpenAlexW3166452193

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.