The Binomial "Inflammation-Epigenetics" in Breast Cancer Progression and Bone Metastasis: IL-1β Actions Are Influenced by TET Inhibitor in MCF-7 Cell Line

被引:15
作者
Bellavia, Daniele [1 ]
Costa, Viviana [1 ]
De Luca, Angela [1 ]
Cordaro, Aurora [1 ]
Fini, Milena [2 ]
Giavaresi, Gianluca [1 ]
Caradonna, Fabio [3 ]
Raimondi, Lavinia [1 ]
机构
[1] IRCCS Ist Ortoped Rizzoli, SC Sci & Tecnol Chirurg STC, I-40136 Bologna, Italy
[2] IRCCS Ist Ortoped Rizzoli, Direz Scientif, I-40136 Bologna, Italy
[3] Univ Palermo, Dipartimento Sci & Tecnol Biol Chim & Farmaceut, Viale Sci, Edificio 16, I-90128 Palermo, Italy
关键词
DNA methylation; bone metastasis; inflammation; Interleukin-1; beta; ten-eleven translocation proteins; MCF-7 cell line; METHYLATION; CYTOKINES; RECEPTOR;
D O I
10.3390/ijms232315422
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 demethylating 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-1 beta-dependent tumor progression and bone metastasis formation.
引用
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页数:15
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