ArticleDiscover oncology2026
FABP5 confers resistance to drug-induced ROS toxicity in cervical cancer cell lines by suppressing the PPARγ/CPT1A signaling pathway.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.