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

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 fun...

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Main Authors: Dijie Zheng, Yazhu Deng, Lu Deng, Zhiwei He, Xinghao Sun, Yanyu Gong, Binbin Shi, Deqin Lu, Chao Yu
Format: Article
Language:English
Published: Nature Publishing Group 2025-02-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07399-1
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author Dijie Zheng
Yazhu Deng
Lu Deng
Zhiwei He
Xinghao Sun
Yanyu Gong
Binbin Shi
Deqin Lu
Chao Yu
author_facet Dijie Zheng
Yazhu Deng
Lu Deng
Zhiwei He
Xinghao Sun
Yanyu Gong
Binbin Shi
Deqin Lu
Chao Yu
author_sort Dijie Zheng
collection DOAJ
description 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.
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institution Kabale University
issn 2041-4889
language English
publishDate 2025-02-01
publisher Nature Publishing Group
record_format Article
series Cell Death and Disease
spelling doaj-art-1b336c788e874ad7b42ab9b4599868962025-02-09T12:56:41ZengNature Publishing GroupCell Death and Disease2041-48892025-02-0116111210.1038/s41419-025-07399-1CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistanceDijie Zheng0Yazhu Deng1Lu Deng2Zhiwei He3Xinghao Sun4Yanyu Gong5Binbin Shi6Deqin Lu7Chao Yu8School of Basic Medical Sciences, Guizhou Medical UniversitySchool of Basic Medical Sciences, Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversitySchool of Basic Medical Sciences, Guizhou Medical UniversityDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Guizhou Medical UniversityAbstract 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.https://doi.org/10.1038/s41419-025-07399-1
spellingShingle Dijie Zheng
Yazhu Deng
Lu Deng
Zhiwei He
Xinghao Sun
Yanyu Gong
Binbin Shi
Deqin Lu
Chao Yu
CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
Cell Death and Disease
title CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
title_full CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
title_fullStr CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
title_full_unstemmed CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
title_short CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
title_sort cdca7 enhances stat3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance
url https://doi.org/10.1038/s41419-025-07399-1
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