Inhibition of the FEN1-PBX1 axis elicits cellular senescence in breast cancer via the increased intracellular reactive oxygen species levels

Knockdown of FEN1 facilitates breast cancer cell senescence through PBX1 down-regulation mediating increase in intracellular ROS levels. This study reveals FEN1 as a negative regulator of cellular senescence and provides support for pro-senescence cancer therapy. Given that FEN1 knockdown exhibited only moderate in vivo effects, these findings underscore the necessity of combining it with senolytic therapy to enhance therapeutic efficacy.

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Publication Details

Journal
Journal of Translational Medicine
Published
2025-02-28
DOI
https://doi.org/10.1186/s12967-025-06216-9
Citations
4
Primary Topic
Epigenetics and DNA Methylation
Type
article
Field-Weighted Citation Impact
3.22

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article

Inhibition of the FEN1-PBX1 axis elicits cellular senescence in breast cancer via the increased intracellular reactive oxygen species levels

Min Wu, Jingjing Liu, Zirui Wang, Xiaoshan Huang et al.
4 citations
Journal of Translational Medicine
Epigenetics and DNA Methylation
3.22
article

Inhibition of the FEN1-PBX1 axis elicits cellular senescence in breast cancer via the increased intracellular reactive oxygen species levels

Min Wu, Jingjing Liu, Zirui Wang, Xiaoshan Huang, Benmeng Wu, Yaqin Zhu, Lin Yu, Miaolin Zhu
article en
4 citations

Abstract

Knockdown of FEN1 facilitates breast cancer cell senescence through PBX1 down-regulation mediating increase in intracellular ROS levels. This study reveals FEN1 as a negative regulator of cellular senescence and provides support for pro-senescence cancer therapy. Given that FEN1 knockdown exhibited only moderate in vivo effects, these findings underscore the necessity of combining it with senolytic therapy to enhance therapeutic efficacy.

Journal of Translational MedicineVol. 23(1)
Jiangsu Cancer Hospital (CN), Yangzhou University (CN)
National Natural Science Foundation of China
Zero hunger
Openalex Percentile: Top 9%
Epigenetics and DNA Methylation
3.22
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