Editorial Volume 11, Issue 18 pp 7336—7338

Figure 1. A model of the function of lamin B1 in the control of lung tumorigenesis and its potential link to aging/senescence. Lamin B1 recruits EZH1/EZH2 to catalyze H3K27me3 and repress the expression of genes, including RET and GFRα1. When lamin B1 is depleted, EZH1/2 recruitment and H3K27me3 marks are reduced, RET/GFRα1 are upregulated and promote lung tumor growth and metastasis. Interference with Ret signaling using available inhibitors (blue blunted arrows) could suppress the growth and progression of lamin B1-deficient lung tumors. Furthermore, aging and cellular senescence are linked to a decrease of lamin B1 in older tissues. Loss of lamin B1 can induce a senescent state that may in turn be linked to certain aspects of tumor progression through secreted factors produced by senescent cells. Such factors might be regulated by lamin B1-EZH1/2-dependent changes in gene expression. Counteracting mechanisms linking senescence to lamin B1 and vice versa may therefore also hamper cancer development and metastasis (blue dashed blunted arrows).