The present study focused on the elucidation of the putative anticancer potential of quercetin. The anticancer activity of quercetin at 10, 20, 40, 80 and 120 µM was assessed in vitro by MMT assay in 9 tumor cell lines (colon carcinoma CT‑26 cells, prostate adenocarcinoma LNCaP cells, human prostate PC3 cells, pheocromocytoma PC12 cells, estrogen receptor‑positive breast cancer MCF‑7 cells, acute lymphoblastic leukemia MOLT‑4 T‑cells, human myeloma U266B1 cells, human lymphoid Raji cells and ovarian cancer CHO cells). Quercetin was found to induce the apoptosis of all the tested cancer cell lines at the utilized concentrations. Moreover, quercetin significantly induced the apoptosis of the CT‑26, LNCaP, MOLT‑4 and Raji cell lines, as compared to control group (P<0.001), as demonstrated by Annexin V/PI staining. In in vivo experiments, mice bearing MCF‑7 and CT‑26 tumors exhibited a significant reduction in tumor volume in the quercetin‑treated group as compared to the control group (P<0.001). Taken together, quercetin, a naturally occurring compound, exhibits anticancer properties both in vivo and in vitro.

The cytochrome P450 (CYP) family is the principal enzyme system involved in the metabolism of xenobiotics and endogenous compounds. Among this family, CYP2A6 is one of the most important enzymes for metabolism of nicotine. In this study, the linkage of CYP2A6*1 and CYP2A6*4 genotypes with nicotine metabolism was investigated. A single polymerase chain reaction-restriction fragment length polymorphism was used to resolve the genotypes into CYP2A6*1 (wild type), CYP2A6*2, or CYP2A6*3. The population studied consisted of 200 healthy smokers from Mashhad city, North East of Iran. The urinary cotinine as the principal metabolite of nicotine was analyzed for 12 subjects (7 subjects with CYP2A6*1 as controls and 5 subjects with CYP2A6*4). The results indicated that cumulative urinary cotinine excretion in CYP2A6*4 genotype was about one-eighth compared with the control group (wild type). Cotinine formation from nicotine has individual and ethnic variability that correlated with the level of CYP2A6 expression. Moreover, urinary cotinine level was drastically lower in CYP2A6*4 subjects than in CYP2A6*1 subjects.