Evidence map›Paper›PMID 39730634›Full record

ArticleScientific reports2024

EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer.

Jianyuan Zeng, Cai Wang, Fiona Ruge, Edison Ke Ji, Tracey A Martin, Andrew J Sanders, Shuqin Jia, Chunyi Hao, Wen G Jiang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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.

Jianyuan ZengSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK.
Cai WangSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK.
Fiona RugeSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK.
Edison Ke JiGastrointestinal Cancer Centre, Peking University Cancer Hospital, Peking University, Fucheng Road, Haidian District, Beijing, China.
Tracey A MartinSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK.
Andrew J SandersSchool of Education and Science, University of Gloucestershire, Francis Close Hall, Swindon Road, Cheltenham, GL50 4AZ, UK.
Shuqin JiaGastrointestinal Cancer Centre, Peking University Cancer Hospital, Peking University, Fucheng Road, Haidian District, Beijing, China.
Chunyi HaoGastrointestinal Cancer Centre, Peking University Cancer Hospital, Peking University, Fucheng Road, Haidian District, Beijing, China.
Wen G JiangSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK. jiangw@cardiff.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most pancreatic cancer patients are diagnosed at advanced stages, with poor survival rates and drug resistance making pancreatic cancer one of the highest causes of cancer death in the UK. Understanding the underlying mechanism behind its carcinogenesis, metastasis and drug resistance has become an essential task for researchers. We have discovered that a well-established tumour suppressor, EPLIN, has an oncogenic rather than suppressive role in pancreatic cancer. Notably, upregulation of EPLIN was observed in pancreatic cancer samples compared to normal samples at RNA and protein levels. Moreover, the presence of EPLIN resulted in poor clinical outcomes in patients. We also report that inhibition of EPLIN led to reduced cellular growth and migration in pancreatic cancer cells. EPLIN regulates expression and phosphorylation levels of several key players in MAPK and PIK3CA-AKT signalling pathways, as well as key contributors of EMT. Furthermore, EPLIN mediates the inhibitory ability PIK3 kinases, MEK and ERK inhibitors have on cell migration. EPLIN was also found to have an impact on pancreatic cancer cells response to chemotherapeutic and EGFR/HER2 targeted therapeutic agents, namely gemcitabine, fluorouracil (5FU) and neratinib (Nerlynx).

Indexed as

Cell MovementCell ProliferationDrug Resistance, NeoplasmPancreatic NeoplasmsAntineoplastic AgentsCell Line, TumorEpithelial-Mesenchymal TransitionFluorouracilGemcitabineGene Expression Regulation, NeoplasticHumansSignal TransductionAntineoplastic AgentsFluorouracilGemcitabineChemotherapeutic resistanceEPLINMAPKMigrationPancreatic cancerPIK3s

Identifiers

PMID39730634
PMCPMC11680852

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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.