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

Ting Zhang1,2, Jiamei Zhu3, Li Geng4

  • 1Department of Obstetrics and Gynecology, The First Afffliated Hospital of Soochow University, Suzhou, 215006, China.

Discover Oncology
|May 25, 2026
PubMed

Insights

Fatty acid-binding protein 5 (FABP5) promotes cervical cancer progression by enhancing cell growth and chemoresistance. It achieves this by increasing cellular energy and reducing reactive oxygen species (ROS) via the PPARγ/CPT1A pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Fatty acid-binding protein 5 (FABP5) is implicated in various cancers.
  • Its specific role in cervical cancer progression and as a therapeutic target requires elucidation.

Purpose of the Study:

  • To investigate the function of FABP5 in cervical squamous cell carcinoma (CESC).
  • To assess FABP5 as a potential clinical treatment target for cervical cancer.

Main Methods:

  • Bioinformatics analysis and immunohistochemistry (IHC) for FABP5 expression.
  • In vitro cell culture, RNA sequencing (RNA-seq), oil red O (ORO) staining.
  • Protein-protein interaction (PPI) network analysis.

Main Results:

  • FABP5 overexpression enhanced CESC cell proliferation, migration, and invasion.
  • FABP5 conferred resistance to cisplatin and paclitaxel chemotherapy.
  • FABP5 regulates cellular metabolism, increasing energy reserves and reducing reactive oxygen species (ROS) by inhibiting PPARγ/CPT1A and ATP5A1 signaling.

Conclusions:

  • FABP5 promotes cervical cancer progression and chemoresistance.
  • FABP5 maintains cellular energy reserves and a low-ROS state by inhibiting the PPARγ/CPT1A pathway and downregulating ATP5A1.
  • The PPARγ/CPT1A pathway is a key mechanism for cellular defense against ROS.

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