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<p>Fatty acid-binding protein 5 (FABP5) is highly expressed in various tumor cell types and is associated with cancer progression. The aim of this study is to clarify the role of FABP5 in cervical cancer to determine its potential value as a clinical treatment target. Online bioinformatics platforms and immunohistochemistry (IHC) were used to analyze FABP5 expression and function in cervical squamous cell carcinoma (CESC). In vitro experiments revealed that overexpression of FABP5 significantly enhanced the proliferation, migration, and invasion abilities of cervical cancer cells. Moreover, resistance to the killing effects of cisplatin and paclitaxel was observed. RNA sequencing (RNA-seq) results and oil red cell (ORO) staining experiments revealed the key role of FABP5 in cellular metabolism. Protein‒protein interaction (PPI) network analysis revealed that by inhibiting the activation of the key lipid regulation signaling pathways PPARγ/CPT1A and ATP5A1, overexpression of FABP5 not only increased the energy reserves of cells but also reduced the level of reactive oxygen species (ROS) produced by fatty acid β-oxidation. Further experiments revealed that exogenous drugs could reduce the cellular energy reserve and activate PPARγ/CPT1A and ATP5A1. In conclusion, FABP5 increases cellular energy reserves while maintaining cells in a low-ROS state by inhibiting PPARγ/CPT1A signaling and downregulating the expression of the respiratory chain component ATP5A1. The PPARγ/CPT1A signaling pathway may represent one of the key mechanisms through which cells defend against exogenous ROS.</p>

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FABP5 confers resistance to drug-induced ROS toxicity in cervical cancer cell lines by suppressing the PPARγ/CPT1A signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月25日

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  • Ting Zhang,
  • Jiamei Zhu,
  • Li Geng,
  • Zhixing Jin,
  • Zhijia Xie,
  • Wei Liu,
  • Mei Yang,
  • Hongmei Ding,
  • Youguo Chen

摘要

Fatty acid-binding protein 5 (FABP5) is highly expressed in various tumor cell types and is associated with cancer progression. The aim of this study is to clarify the role of FABP5 in cervical cancer to determine its potential value as a clinical treatment target. Online bioinformatics platforms and immunohistochemistry (IHC) were used to analyze FABP5 expression and function in cervical squamous cell carcinoma (CESC). In vitro experiments revealed that overexpression of FABP5 significantly enhanced the proliferation, migration, and invasion abilities of cervical cancer cells. Moreover, resistance to the killing effects of cisplatin and paclitaxel was observed. RNA sequencing (RNA-seq) results and oil red cell (ORO) staining experiments revealed the key role of FABP5 in cellular metabolism. Protein‒protein interaction (PPI) network analysis revealed that by inhibiting the activation of the key lipid regulation signaling pathways PPARγ/CPT1A and ATP5A1, overexpression of FABP5 not only increased the energy reserves of cells but also reduced the level of reactive oxygen species (ROS) produced by fatty acid β-oxidation. Further experiments revealed that exogenous drugs could reduce the cellular energy reserve and activate PPARγ/CPT1A and ATP5A1. In conclusion, FABP5 increases cellular energy reserves while maintaining cells in a low-ROS state by inhibiting PPARγ/CPT1A signaling and downregulating the expression of the respiratory chain component ATP5A1. The PPARγ/CPT1A signaling pathway may represent one of the key mechanisms through which cells defend against exogenous ROS.