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2023 World Conference on Lung Cancer (Posters)
P1.12. BiFeO3@PANI Sensitizes LKB1-Deficient LUAD ...
P1.12. BiFeO3@PANI Sensitizes LKB1-Deficient LUAD to Radiotherapy via Induction of Tumoral Lipid Oxidation and Ferroptosis - PDF(Slides)
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The study investigated the role of BiFeO3@PANI in sensitizing LKB1-deficient lung adenocarcinoma (LUAD) to radiotherapy. The researchers analyzed single cell RNA-seq data from KrasG12D genetically engineered mouse models with Lkb1 or p53 deletion. The analysis revealed that the profiles of tumor-infiltrating lymphocytes were reprogrammed in Lkb1-deletion lung tumors, with fewer neutrophils and more B cells identified. Gene set enrichment analysis predicted that LKB1 deletion altered ferroptosis (a type of programmed cell death) and lipid homeostasis.<br /><br />Using the CTRP database, the researchers identified 17 genes related to ferroptosis resistance, with positive correlations found between LKB1 mutation and high ferroptosis resistance scores in the TCGA-LUAD datasets. In vitro experiments showed that LKB1-deficient cells exhibited less lipid oxidation and were less sensitive to ferroptosis agonists. However, treatment with BiFeO3@PANI increased lipid oxidation and reduced cell proliferation, suggesting that it could overcome the resistance to ferroptosis induced by radiotherapy in LKB1-deficient LUAD.<br /><br />The study provides insights into the mechanisms underlying LUAD resistance to radiotherapy and highlights the potential of BiFeO3@PANI as a sensitizer to enhance the therapeutic effects of radiotherapy in LKB1-deficient LUAD. These findings contribute to the development of more effective treatment strategies for LUAD patients with LKB1 mutations. Further studies are needed to validate these results and explore the clinical implications of targeting ferroptosis in LUAD.
Asset Subtitle
Zeqin Guo
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Speaker
Zeqin Guo
Topic
Tumor Biology: Translational Biology - Translational Therapeutics
Keywords
BiFeO3@PANI
sensitizing
LKB1-deficient lung adenocarcinoma
radiotherapy
single cell RNA-seq data
KrasG12D genetically engineered mouse models
Lkb1 deletion
tumor-infiltrating lymphocytes
ferroptosis
lipid homeostasis
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