Evidence map›Paper›PMID 39905019›Full record

ArticleCell death & disease2025

CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance.

Dijie Zheng, Yazhu Deng, Lu Deng, Zhiwei He, Xinghao Sun, Yanyu Gong, Binbin Shi, Deqin Lu, Chao Yu

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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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

9 authors.

Dijie Zheng *School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou Province, 550025, China.
Yazhu Deng *School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou Province, 550025, China.
Lu Deng *Department of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China.
Zhiwei HeDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China.
Xinghao SunDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China.
Yanyu GongDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China.
Binbin ShiDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China.
Deqin LuSchool of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou Province, 550025, China. dqlu91@hotmail.com.
Chao YuDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, 550001, China. yuchao2002@gmc.edu.cn.ORCID 0000-0002-9244-9416

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82360519
6 · The paper itself

Abstract

Cell division cycle associated 7 (CDCA7) plays a role in various malignancies, especially pancreatic cancer (PC). However, its expression pattern and functional significance in PC require further research. Therefore, this study aimed to investigate CDCA7 expression levels and biological functions in PC using in vitro and in vivo experiments. Western blotting, immunohistochemistry, and real-time polymerase chain reaction were performed to detect CDCA7 expression in PC cells and tissues. Additionally, the biological functions of CDCA7 were assessed using cell proliferation, wound healing, and Transwell assays. CDCA7 overexpression promoted PC cell proliferation, migration, and invasion, and increased resistance to the chemotherapy drug gemcitabine, possibly through enhanced aerobic glycolysis. Additionally, immunoprecipitation assay showed that CDCA7 interacted with STAT3 protein and affected the transcriptional regulation of hexokinase 2. Conclusively, targeting CDCA7 might be a promising therapeutic strategy to increase gemcitabine sensitivity by inhibiting glycolysis in PC cells.

Indexed as

Cell Cycle ProteinsDeoxycytidineDrug Resistance, NeoplasmGlycolysisPancreatic NeoplasmsSTAT3 Transcription FactorAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGemcitabineGene Expression Regulation, NeoplasticHexokinaseHumansCell Cycle ProteinsDeoxycytidineGemcitabineHexokinaseSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID39905019
PMCPMC11794584

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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.