Evidence mapPaperPMID 41812062Full record

ArticlePancreas2026

Knockdown of Lymphoid Enhancer-binding Factor 1 Inhibits Pancreatic Adenocarcinoma Growth and Neoangiogenesis by Curbing Notch1 and Nuclear Factor Kappa B Signaling Pathways.

Guanglun Ping, Guoyong Cai, Ying Wei, Xiangli Mo, Li Liu, Wencui Zhu, Yi Zhang

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Article in Pancreas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Guanglun PingDepartment of Gastroenterology.
Guoyong CaiDepartment of Gastroenterology.
Ying WeiDepartment of Gastroenterology.
Xiangli MoDepartment of Nursing.
Li LiuDepartment of Nursing.
Wencui ZhuDepartment of Pathology.
Yi ZhangDepartment of Nephrology, Wenshan People's Hospital, Wenshan, Yunnan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the impaction of LEF1 for malignant development of pancreatic adenocarcinoma (PAAD) and its specific mechanisms. MATERIALS AND

methodsThe expression of LEF1 in PAAD and normal tissues was inspected by bioinformatics, qRT-PCR, and western blot (WB). AsPC-1 and BxPC-3 were selected for further knockdown study. The post-knockdown cellular malignant progression was evaluated by CCK-8, EdU, clonogenic assay, wound healing, Transwell, Calcein AM/PI staining, and LDH release assays. Conditioned medium (CM) of PAAD after LEF1 knockdown was collected to culture HUVEC for evaluating the effect on angiogenesis. Immunofluorescence assay and WB were employed to detect the changes of Notch1 and NF-κB pathway. Finally, a nude mouse tumor xenograft model was established to verify the in vivo suppressive effect of knocking down LEF1 on PAAD.

resultsLEF1 is highly expressed in PAAD. The proliferation, migration, and invasion of AsPC-1/sh-LEF1 and BxPC-3/sh-LEF1 were inhibited, and the apoptosis was significantly increased. The CM of AsPC-1/sh-LEF1 and BxPC-3/sh-LEF1 significantly inhibited HUVEC migration and angiogenesis. The intranuclear expression of Notch1, NICD, Hes1, and P65 proteins were reduced, indicating that LEF1 downregulation inhibited the activation of the Notch1 and NF-κB. Finally, the inhibitory effect of LEF1 downregulation on PAAD growth was further verified in vivo, confirming the important role of LEF1 in PAAD development.

conclusionsKnockdown of LEF1 can inhibit the growth and neoangiogenesis of PAAD by inhibiting Notch1 and NF-κB, thus inhibiting the malignant progression of PAAD.

Indexed as

AdenocarcinomaLymphoid Enhancer-Binding Factor 1Neovascularization, PathologicNF-kappa BPancreatic NeoplasmsReceptor, Notch1AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsMaleLEF1 protein, humanLymphoid Enhancer-Binding Factor 1NF-kappa BNOTCH1 protein, humanReceptor, Notch1LEF1neovascularizationNF-κBNotch1PAAD

Identifiers

PMID41812062
PMCPMC12975020

What Socratic holds

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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 Socratic graph.