Evidence map›Paper›PMID 40596639›Full record

ArticleJournal of cellular and molecular medicine2025

The Key Role of COA6 in Pancreatic Ductal Adenocarcinoma: Metabolic Reprogramming and Regulation of the Immune Microenvironment.

Lai Jiang, Yuxuan Jiang, Xuancheng Zhou, Lexin Wang, Shengke Zhang, Chenglu Jiang, Hui Meng, Qingwen Hu, Yuheng Gu, Yipin Fu and 3 more

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

13 authors.

Lai JiangWestern Institute of Digital-Intelligent Medicine, Chongqing, China.
Yuxuan JiangSouthwest Medical University, Luzhou, China.ORCID 0009-0009-2152-5512
Xuancheng ZhouSouthwest Medical University, Luzhou, China.
Lexin WangWestern Institute of Digital-Intelligent Medicine, Chongqing, China.
Shengke ZhangSouthwest Medical University, Luzhou, China.
Chenglu JiangSouthwest Medical University, Luzhou, China.
Hui MengDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Qingwen HuSouthwest Medical University, Luzhou, China.
Yuheng GuSouthwest Medical University, Luzhou, China.
Yipin FuSouthwest Medical University, Luzhou, China.
Ke XuDepartment of Oncology, Chongqing General Hospital, Chongqing University, Chongqing, China.
Hao ChiWestern Institute of Digital-Intelligent Medicine, Chongqing, China.ORCID 0000-0002-5210-0770
Xiaolin ZhongDepartment of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China.

Funding

Natural Science Foundation of Sichuan Province 2022NSFSC1378Sichuan Medical Science and Technology Innovation Research Association (abbreviated as Sichuan Medical Innovation Association) launched the "; Summit of Medical Innovation" Special Research Project. 2025.01-2027.03 YCH-KY-YCZD2024-298Sichuan Provincial Department of Science and Technology Research Project. 2022.01-2024.12 2022YFS0633Wellcome Trust 202401
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterised by immune hypo-responsiveness due to its complex, immunosuppressive tumour microenvironment (TME). Mitochondrial metabolic reprogramming allows PDAC cells to shift between glycolysis and oxidative phosphorylation (OXPHOS), supporting energy production and cellular viability, thus promoting tumour progression and therapeutic resistance. Mitochondrial genes associated with PDAC were identified using SMR/HEIDI analysis combined with MRC IEU OpenGWAS and GTEx V8 pancreatic eQTL databases. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics were used to explore cellular interactions and construct spatial interaction networks. Potential small-molecule compounds targeting the TME were identified through drug prediction and molecular docking. COA6 expression was silenced in SW1990 and PANC-1 cells to assess effects on cell proliferation, migration, invasion and apoptosis. COA6, a key gene in the OXPHOS pathway, was upregulated in PDAC tumours compared to normal tissues. Functional assays showed that COA6 overexpression enhanced proliferation, migration and chemoresistance of PDAC cells. COA6 modulates OXPHOS, influences the TME and promotes drug resistance in PDAC. It is a promising therapeutic target for improving clinical outcomes in PDAC patients. Further research is needed to develop COA6-targeted therapies.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsTumor MicroenvironmentApoptosisCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGlycolysisHumansMetabolic ReprogrammingMitochondriaOxidative Phosphorylationmitochondrial dysfunctionpancreatic ductal adenocarcinomasingle‐cell analysisspatial transcriptomicstumour immunology

Identifiers

PMID40596639
PMCPMC12213452

What OpenQuestion holds

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LicenceCC BY
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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.