[Retracted] Analysis and Validation of Differentially Expressed Ferroptosis‐Related Genes in Regorafenib‐Induced Cardiotoxicity
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Post-publication record
- Nature
- Retraction
- Reason
- Compromised Peer Review;Investigation by Journal/Publisher;Investigation by Third Party;Paper Mill;Unreliable Results and/or Conclusions;
- Date
- 12/29/2023 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
Background: Although tyrosine kinase inhibitors (TKIs) constitute a type of anticancer drugs, the underlying mechanisms of TKI-associated cardiotoxicity remain largely unknown. Ferroptosis is a regulated cell death form that implicated in several tumors' biological processes. Our objective was to probe into the differential expression of ferroptosis-related genes in regorafenib-induced cardiotoxicity through multiple bioinformatics analysis and validation. Methods and Materials: (V.3.6.3). Then, Gene Ontology (GO) Enrichment Analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) Enrichment Analysis, and Gene Set Enrichment Analysis (GSEA) were used to explore DEGs' bioinformatics functions and enriched pathways. We intersected DEGs with 259 ferroptosis-related genes from the FerrDb database. Finally, the mRNA levels of differentially expressed ferroptosis-related genes (DEFRGs) were validated in regorafenib-cultured cardiomyocytes to anticipate the link between DEFRGs and cardiotoxicity. Results: 747,1127,773 and 969 DEGs were screened out in adult human cardiomyocyte lines A, B, D, and E, respectively. The mechanism by which REG promotes cardiotoxicity associated with ferroptosis may be regulated by PI3K-Akt, TGF-beta, and MAPK. GSEA demonstrated that REG can promote cardiotoxicity by suppressing genes and pathways encoding extracellular matrix and related proteins, oxidative phosphorylation, or ATF-2 transcription factor network. After overlapping DEGs with ferroptosis-related genes, we got seven DEFRGs and found that ATF3, MT1G, and PLIN2 were upregulated and DDIT4 was downregulated. The ROC curve demonstrated that these genes predict regorafenib-induced cardiotoxicity well. Conclusion: We identified four DEFRGs which may become potential predictors and participate in the regorafenib-induced cardiotoxicity. Our findings provide possibility that targeting these ferroptosis-related genes may be an alternative for clinical prevention and therapy of regorafenib-related cardiotoxicity.
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The record
- Venue
- Oxidative Medicine and Cellular Longevity
- Topic
- Ferroptosis and cancer prognosis
- Field
- Medicine
- Canadian institutions
- Queen's University
- Funders
- Natural Science Foundation of Heilongjiang ProvinceHeilongjiang Provincial Postdoctoral Science FoundationMinistry of Education of the People's Republic of ChinaNational Natural Science Foundation of ChinaHarbin Medical University
- Keywords
- RegorafenibCardiotoxicityGeneBiologyComputational biologyCancer researchGeneticsCancerColorectal cancerChemotherapy
- Has abstract in OpenAlex
- yes