Evidence map›Paper›PMID 35197444›Full record

ArticleCell death & disease2022

Numb-PRRL promotes TGF-β1- and EGF-induced epithelial-to-mesenchymal transition in pancreatic cancer.

Weiwei Sheng, Jingtong Tang, Rongxian Cao, Xiaoyang Shi, Yuteng Ma, Ming Dong

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Inflammation, microbiota, and pancreatic cancer.Cancer cell international · 2025
    Review
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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

6 authors at 2 institutions in 1 country.

Weiwei ShengDepartment of Gastrointestinal Surgery, The First Hospital, China Medical University, 110001, Shenyang, Liaoning, China.
Jingtong TangDepartment of Gastrointestinal Surgery, The First Hospital, China Medical University, 110001, Shenyang, Liaoning, China.
Rongxian CaoDepartment of Gastrointestinal Surgery, The First Hospital, China Medical University, 110001, Shenyang, Liaoning, China.
Xiaoyang ShiDepartment of Hernia and Abdominal Wall Surgery, Chaoyang Hospital, 100043, Beijing, China.
Yuteng MaDepartment of Gastrointestinal Surgery, The First Hospital, China Medical University, 110001, Shenyang, Liaoning, China.
Ming DongDepartment of Gastrointestinal Surgery, The First Hospital, China Medical University, 110001, Shenyang, Liaoning, China. dongming@cmu.edu.cn.ORCID 0000-0003-2685-1420
First Hospital of China Medical University · CNBeijing Chaoyang Emergency Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isoform-specific functions of Numb in the development of cancers, especially in the initiation of epithelial-to-mesenchymal transition (EMT) remains controversial. We study the specific function of Numb-PRRL isoform in activated EMT of pancreatic ductal adenocarcinoma (PC), which is distinguished from our previous studies that only focused on the total Numb protein. Numb-PRRL isoform was specifically overexpressed and silenced in PC cells combining with TGF-β1 and EGF stimulus. We systematically explored the potential effect of Numb-PRRL in the activated EMT of PC in vitro and in vivo. The total Numb protein was overexpressed in the normal pancreatic duct and well-differentiated PC by IHC. However, Numb-PRRS isoform but not Numb-PRRL showed dominant expression in PC tissues. Numb-PRRL overexpression promoted TGF-β1-induced EMT in PANC-1 and Miapaca-2 cells. TGF-β1-induced EMT-like cell morphology, cell invasion, and migration were enhanced in Numb-PRRL overexpressing groups following the increase of N-cadherin, Vimentin, Smad2/3, Snail1, Snail2, and cleaved-Notch1 and the decrease of E-cadherin. Numb-PRRL overexpression activated TGFβ1-Smad2/3-Snail1 signaling was significantly reversed by the Notch1 inhibitor RO4929097. Conversely, Numb-PRRL silencing inhibited EGF-induced EMT in AsPC-1 and BxPC-3 cells following the activation of EGFR-ERK/MAPK signaling via phosphorylating EGFR at tyrosine 1045. In vivo, Numb-PRRL overexpression or silencing promoted or inhibited subcutaneous tumor size and distant liver metastases via regulating EMT and Snail signaling, respectively. Numb-PRRL promotes TGF-β1- and EGF-induced EMT in PC by regulating TGF-β1-Smad2/3-Snail and EGF-induced EGFR-ERK/MAPK signaling.

Indexed as

Epithelial-Mesenchymal TransitionMembrane ProteinsNerve Tissue ProteinsPancreatic NeoplasmsTransforming Growth Factor beta1Cell Line, TumorCell MovementEpidermal Growth FactorErbB ReceptorsHumansEpidermal Growth FactorErbB ReceptorsMembrane ProteinsNerve Tissue ProteinsNUMB protein, humanTransforming Growth Factor beta1

Identifiers

PMID35197444
PMCPMC8866481
OpenAlexW4214553643

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.