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. Author manuscript; available in PMC: 2009 Oct 7.
Published in final edited form as: Cancer Cell. 2008 Oct 7;14(4):312–323. doi: 10.1016/j.ccr.2008.09.001

Figure 6. SIRT1 deficiency causes genomic instability and tumor formation.

Figure 6

(A) Tumor free curve of different genotypes mice, including SIRT1+/−p53+/− (n=49), p53+/− (n=12), SIRT1+/− (n=37), and WT (n=18). (B) Types and percentage of tumors developed in SIRT1+/−p53+/− mice. (C) Chromosome spread from a mammary tumor. Regardless of the tumor type, general events are aneuploidy, numerous structural chromosomal aberrations, and premature chromosome segregation. Arrow points to abnormally long chromosome created by end fusion. (D) SKY analysis on metaphase spreads from a primary tumor, showing non-reciprocal translocation (T(13;2)(C3-D1)), a complex non-reciprocal translocation (T(10;410)), dicentric chromosomes, and a variety of chromosomal fragments from chromosomes 1,2, 4, 8, 10 and 19 respectively. (E) Treatment of resveratrol reduced tumor incidence in SIRT1+/−p53+/− mice. Resveratrol group treated group consisted of 10 female mice. The control ground contained 10 DMSO treated and 16 untreated female mice. Logrank test: p<0.01. (F) Treatment of resveratrol caused altered expression of several known downstream genes of SIRT1. Data is presented as average ±SD. (G). Western blot analysis showing that all three tumors developed in the resveratrol treated SIRT1+/−p53+/− mice lost SIRT1 expression, while only one out of four tumors in the mock treated mice lost SIRT1 expression. Bar: 10 µm for C.