Evidence map›Paper›PMID 38520747›Full record

ArticleBiomolecules & biomedicine2024

SPDEF drives pancreatic adenocarcinoma progression via transcriptional upregulation of

Hang Jiang, Zhiqian Xue, Liping Zhao, Boyuan Wang, Chenfei Wang, Haihan Song, Jianjun Sun

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules & biomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 2 institutions in 1 country.

Hang JiangDepartment of Hepatobiliary and Pancreatic Surgery, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Zhiqian XueDepartment of Hepatobiliary and Pancreatic Surgery, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Liping ZhaoDepartment of Hepatobiliary and Pancreatic Surgery, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Boyuan WangShanghai Qibao Dwight High School, Shanghhai, China.
Chenfei WangDepartment of Emergency, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Haihan SongDepartment of Hepatobiliary and Pancreatic Surgery, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China; Department of Immunology, DICAT Biomedical Computation Centre, Vancouver, BC, Canada; Central Lab, Shanghai Key Laboratory of Pathogenic Fungi Medical Testing, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Jianjun SunDepartment of Hepatobiliary and Pancreatic Surgery, The Third People's Hospital of Yunnan Province, Kunming, Yunnan, China.
Third People's Hospital of Yunnan Province · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic adenocarcinoma (PAAD) is a notably aggressive malignancy with limited treatment options and an unfavorable prognosis for patients. We aimed to investigate molecular mechanisms by which Sam's pointed domain-containing ETS transcription factor (SPDEF) exerts effects on PAAD progression. We analyzed differentially expressed genes (DEGs) and their integration with ETS family members using the The Cancer Genome Atlas (TCGA) database, hence identifying SPDEF as a core gene in PAAD. Kaplan-Meier survival analysis confirmed SPDEF's prognostic potential. In vitro experiments validated the association with cell proliferation and apoptosis, affecting pancreatic cancer cell dynamics. We detected increased SPDEF expression in PAAD tumor samples. Our in vitro studies revealed that SPDEF regulates mRNA and protein expression levels, and significantly affects cell proliferation. Moreover, SPDEF was associated with reduced apoptosis and enhanced cell migration and invasion. In-depth analysis of SPDEF-targeted genes revealed four crucial genes for advanced prognostic model, among which S100A16 was significantly correlated with SPDEF. Mechanistic analysis showed that SPDEF enhances the transcription of S100A16, which in turn enhances PAAD cell migration, proliferation, and invasion by activating the PI3K/AKT signaling pathway. Our study revealed the critical role of SPDEF in promoting PAAD by upregulating S100A16 transcription and stimulating the PI3K/AKT signaling pathway. This knowledge deepened our understanding of pancreatic cancer's molecular progression and unveiled potential therapeutic strategies targeting SPDEF-driven pathways.

Indexed as

AdenocarcinomaDisease ProgressionGene Expression Regulation, NeoplasticPancreatic NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-etsSignal TransductionUp-RegulationApoptosisCell Line, TumorCell MovementCell ProliferationFemaleHumansMalePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-etsS100A16 protein, humanS100 ProteinsSPDEF protein, human

Identifiers

PMID38520747
PMCPMC11379002
OpenAlexW4393111247

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.