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In breast cancer cell lines (MCF-7), activation of IGF/PI3K signaling enhances mitochondrial homeostasis by increasing the number of new mitochondria and levels of oxidative phosphorylation and promotes the degradation of damaged mitochondria (mitochondrial autophagy) by increasing BNIP3, a protective mechanism that ultimately influences the cancer treatment response and evolution of the cancer phenotype (53)
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HN1 suppresses CTCF transcriptional activation by recruiting histone deacetylase 2 to deacetylate H3K27 at the CTCF promoter, thereby regulating the chromatin accessibility of thyroid differentiation genes
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