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RESEARCH PRODUCT
The Binomial “Inflammation-Epigenetics” in Breast Cancer Progression and Bone Metastasis: IL-1β Actions Are Influenced by TET Inhibitor in MCF-7 Cell Line
Daniele BellaviaViviana CostaAngela De LucaAurora CordaroMilena FiniGianluca GiavaresiFabio CaradonnaLavinia Raimondisubject
Epithelial-Mesenchymal TransitionDNA methylation; bone metastasis; inflammation; Interleukin-1β; ten-eleven translocation proteins; MCF-7 cell lineInterleukin-1betaBreast NeoplasmsBone NeoplasmsMCF-7 cell lineCatalysisEpigenesis GeneticInorganic ChemistrySettore BIO/13 - Biologia ApplicataCell Line TumorHumansPhysical and Theoretical ChemistryMolecular BiologySpectroscopybone metastasisDNA methylationten-eleven translocation proteinsOrganic ChemistryGeneral MedicineInterleukin-1βComputer Science ApplicationsSettore BIO/18 - GeneticainflammationMCF-7 CellsFemaleInflammatory Breast Neoplasmsdescription
The existence of a tight relationship between inflammation and epigenetics that in primary breast tumor cells can lead to tumor progression and the formation of bone metastases was investigated. It was highlighted how the induction of tumor progression and bone metastasis by Interleukin-1 beta, in a non-metastatic breast cancer cell line, MCF-7, was dependent on the de-methylating actions of ten-eleven translocation proteins (TETs). In fact, the inhibition of their activity by the Bobcat339 molecule, an inhibitor of TET enzymes, determined on the one hand, the modulation of the epithelial-mesenchymal transition process, and on the other hand, the reduction in the expression of markers of bone metastasis, indicating that the epigenetic action of TETs is a prerequisite for IL-1β-dependent tumor progression and bone metastasis formation.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2022-12-06 | International Journal of Molecular Sciences |