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. 2015 Dec 30;7(5):5598–5612. doi: 10.18632/oncotarget.6798

Figure 5. ENO1 silencing induces cellular senescence.

Figure 5

A. Senescence-associated β-galactosidase staining. Senescent PT45, MDA-MB-231 and NCI-H441 cells were colored blue upon X-gal staining at pH 6. One representative out of three independent experiments is shown. B.–D. Effects of antioxidants on shENO1 cells. After a 7-day treatment with anti-oxidant N-acetyl-cysteine (NAC) or 6-Hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (TROLOX-C), PT45 cells were stained with X-gal at pH 6 to detect the presence of senescent cells. One representative out of three independent experiments is shown (B). Cell growth was assessed after treatment with NAC (C) or TROLOX-C (D). Bars represent fold-increase in number of cells relative to untreated shCTRL (white bars) or shENO1 (black bars) cells. E.–F. Analysis of glutamine amidophosphoribosyltransferase (GPAT) (E) and carbamoyl phosphate synthetase II (CPSII) (F) activity in CFPAC-1, MDA-MB-231 and NCI-H441 cell lines after treatment with NAC or TROLOX-C. GPAT activity is expressed as pmol glutamate/h/mg protein. CPSII activity is expressed as pmol carbamoyl aspartate/min/mg. Results are means of three independent experiments ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 relative to shCTRL. G. In vivo growth of shCTRL (white circles) or shENO1 (black circles) CFPAC-1 (left panel) or MDA-MB-231 (right panel) injected s.c. in SCID-beige mice. The graph represents the mean tumor volume (n = 5 mice/group). Curves were compared by two-way ANOVA, ***p < 0.001.