Evidence map›Paper›PMID 33955688›Full record

ArticleJournal of cellular and molecular medicine2021

Neutrophil extracellular DNA traps promote pancreatic cancer cells migration and invasion by activating EGFR/ERK pathway.

Wei Jin, Huijing Yin, Hao Li, Xian-Jun Yu, Hua-Xiang Xu, Liang Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Leveraging Microphysiological Systems to Facilitate Neutrophil-Based Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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6 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Wei JinShanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-3639-1547
Huijing YinTranslational Medicine Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hao LiDepartment of Pancreatic Surgery, Pancreatic Cancer Institute, Fudan University, Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Shanghai, China.
Xian-Jun YuDepartment of Pancreatic Surgery, Pancreatic Cancer Institute, Fudan University, Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Shanghai, China.
Hua-Xiang XuDepartment of Pancreatic Surgery, Pancreatic Cancer Institute, Fudan University, Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Shanghai, China.
Liang LiuDepartment of Pancreatic Surgery, Pancreatic Cancer Institute, Fudan University, Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Shanghai, China.
Fudan University Shanghai Cancer Center · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 81601985National Natural Science Foundation of China 81802380
6 · The paper itself

Abstract

Neutrophil extracellular DNA traps (NETs) are newly discovered forms of activated neutrophils. Increasing researches have shown that NETs play important roles in cancer progression. Our previous study has proved that tumour-infiltrating NETs could predict postsurgical survival in patients with pancreatic ductal adenocarcinoma (PDAC). However, the roles of NETs on the progression of pancreatic cancer are unknown. Here, we investigated the effects of NETs on pancreatic cancer cells. Results showed that both PDAC patients' and normal individuals' neutrophils-derived NETs could promote migration and invasion of pancreatic cancer cells with epithelial-mesenchymal transition. Further, study confirmed that EGFR/ERK pathway played an important role in this progression. The addition of neutralizing antibodies for IL-1β could effectively block the activation of EGFR/ERK companied with reduction of EMT, migration and invasion. Taken together, NETs facilitated EMT, migration and invasion via IL-1β/EGFR/ERK pathway in pancreatic cancer cells. Our study suggests that NETs may provide promising therapeutic targets for pancreatic cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisCell MovementCell ProliferationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesExtracellular TrapsFemaleHumansMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeutrophilsPancreatic NeoplasmsEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesEMTIL-1βNETsPancreatic Cancer

Identifiers

PMID33955688
PMCPMC8184670
OpenAlexW3158550505

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.