Evidence map›Paper›PMID 38229038›Full record

ArticleBMC cancer2024

NUSAP1 promotes pancreatic ductal adenocarcinoma progression by drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation.

Yuan Liu, Rong Tang, Qing-Cai Meng, Si Shi, Jin Xu, Xian-Jun Yu, Bo Zhang, Wei Wang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The role and therapeutic value of NUSAP1 in human cancers.Journal of translational medicine · 2025
    Review
  5. Article
  6. Article
  7. The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. 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

8 authors at 3 institutions in 1 country.

Yuan LiuDepartment of Endoscopy, Fudan University Shanghai Cancer Center, Shanghai, China.
Rong TangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Qing-Cai MengDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Si ShiDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Jin XuDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Xian-Jun YuDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Bo ZhangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. zhangbo@fudanpci.org.
Wei WangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. wangwei@fudanpci.org.
Fudan University Shanghai Cancer Center · CNShanghai Cancer Institute · CNShanghai Medical College of Fudan University · CN

Funding

Clinical Research Plan of Shanghai Hospital Development Center SHDC2020CR1006AScientific Innovation Project of Shanghai Education Committee 2019-01-07-00-07-E00057Shanghai Municipal Science and Technology Major Project 21JC1401500the National Natural Science Foundation of China U21A20374Xuhui District Artificial Intelligence Medical Hospital Cooperation Project 2021-011
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, and its molecular mechanisms are unclear. Nucleolar and spindle-associated protein 1 (NUSAP1), an indispensable mitotic regulator, has been reported to be involved in the development of several types of tumors. The biological function and molecular mechanism of NUSAP1 in PDAC remain controversial. This study explored the effects and mechanism of NUSAP1 in PDAC.

methodsDifferentially expressed genes (DEGs) were screened. A protein‒protein interaction (PPI) network was constructed to identify hub genes. Experimental studies and tissue microarray (TMA) analysis were performed to investigate the effects of NUSAP1 in PDAC and explore its mechanism.

resultsNetwork analysis revealed that NUSAP1 is an essential hub gene in the PDAC transcriptome. Genome heterogeneity analysis revealed that NUSAP1 is related to tumor mutation burden (TMB), loss of heterozygosity (LOH) and homologous recombination deficiency (HRD) in PDAC. NUSAP1 is correlated with the levels of infiltrating immune cells, such as B cells and CD8 T cells. High NUSAP1 expression was found in PDAC tissues and was associated with a poor patient prognosis. NUSAP1 promoted cancer cell proliferation, migration and invasion, drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation.

conclusionsNUSAP1 is an essential hub gene that promotes PDAC progression and leads to a dismal prognosis by drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAMP-Activated Protein KinasesEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMicrotubule-Associated ProteinsPhosphorylationPrognosisAMP-Activated Protein KinasesMicrotubule-Associated ProteinsNUSAP1 protein, humanPRKAA1 protein, humanDifferentially expressed genesFunctional enrichment analysisPancreatic ductal adenocarcinomaProtein‒protein interactionSurvival analysis

Identifiers

PMID38229038
PMCPMC10790387
OpenAlexW4390911030

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.