Evidence map›Paper›PMID 41452572›Full record

ArticleMedical oncology (Northwood, London, England)2025

Role of Aldo-Keto reductase family 1 member C in cancer progression: a special focus on the role of AKR1C1 in pancreatic cancer.

Degao Huang, Heyang Zhang, Yu Zhang, Congliang Chen, Kexin Lin, Xia Wang, Peipei Wang

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2025. 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

7 authors.

Degao HuangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Heyang ZhangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Yu ZhangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Congliang ChenWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Kexin LinWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Xia WangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China. xiawang@scu.edu.cn.
Peipei WangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China. peipeiwang@scu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AKR1Cs, as a reductase enzyme family, play a pro-carcinogenic role in various types of cancers, including hormone-related malignancies and non-hormonal tumors. However, there exists a notable scarcity of literature concerning AKR1Cs expression in pancreatic cancer and the subsequent impacts on its progression. Analyzing pancreatic cancer database information by employing advanced bioinformatics techniques to unravel AKR1Cs' intricate involvement in cancer malignancy, their correlation with clinical pathology, prognostic implications, as well as their responsiveness to conventional and immune-based therapies. Furthermore, the role of AKR1C1 in promoting the malignant progression of pancreatic cancer cell lines was validated using cell proliferation assays (EdU labeling and colony formation), and cell migration and invasion experiments including scratch wound healing and Transwell migration/invasion assays. AKR1Cs are not only significantly overexpressed in pancreatic cancer, but also closely associated with poor clinical grading, clinical chemoresistance and poor immune response in pancreatic cancer.Moreover, regulating the expression of AKR1C1 in pancreatic cancer cells will affect its proliferation, migration, invasion and the occurrence of epithelial-mesenchymal transformation (EMT). Our findings are expected to establish AKR1Cs, especially AKR1C1 as a promising therapeutic target for the clinical treatment of pancreatic cancer.

Indexed as

20-Hydroxysteroid DehydrogenasesPancreatic NeoplasmsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansPrognosis20-Hydroxysteroid Dehydrogenases3 alpha-beta, 20 beta-hydroxysteroid dehydrogenaseBiomarkers, TumorAldo-keto reductases family 1 member cCancer progressionCancer treatmentPancreatic cancerTumor microenvironment

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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.