Figure 4. Taxol treatment alters several cellular metabolic pathways and induces autophagy and senescence in hTERTBJ1 fibroblasts. (A) Summary of changes observed in the expression of numerous metabolic enzymes after treatment with taxol for 48 h, as measured by quantitative proteomics. Taxol treatment increased the expression of enzymes involved in glycolysis, pentose phosphate, and hexosamine biosynthesis and lipid synthesis pathways in detriment of those involved in gluconeogenesis and mitochondrial metabolism (TCA cycle, oxidative phosphorylation, and mitochondrial β–oxidation). Enzymes that show amplified expression after taxol treatment are shown in red, and enzymes that are decreased are shown in green. Cellular metabolic pathways that may be up-regulated are boxed in red, and those that may be down-regulated are boxed in green. (B) Summary of changes observed in the expression of numerous autophagy and senescence-related proteins after treatment with taxol for 48 h, as measured by quantitative proteomics. Taxol amplified the expression of proteins involved in senescence, autophagy, mitophagy and vesicle formation and trafficking. Proteins that show increased expression after treatment are shown in red. (C) Ingenuity Pathway Analysis of azathioprine and taxol-treated hTERT-BJ1 fibroblasts predicted p53, TFEB and CCL5 to be activated in these cells.