Yu Jinsheng, Marsh Sharon, Ahluwalia Ranjeet, McLeod Howard L
Department of Medicine, Washington University School of Medicine and the Siteman Cancer Center, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Cancer Res. 2003 Oct 1;63(19):6170-3.
Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress. With TaqMan real-time quantitative reverse transcription-PCR, this study established a significant difference in FDXR relative RNA expression level between tumor (median, 212.9 units) and normal tissues (median, 113.8 units) from 51 colorectal cancer patients (P < 0.001). Seven single nucleotide polymorphisms (SNPs) in the FDXR gene were discovered, with no significant difference in variant allele frequency between colon tumor and normal tissues (P > 0.05), and the common haplotypes for FDXR were not different between colon tumor and normal samples. No correlation was observed between FDXR genotype and RNA expression implying that the polymorphisms described in this study are not regulating FDXR expression in colon cancer. This genomic characterization provides the foundation for pharmacogenetic analysis of the impact of FDXR on chemotherapy for colorectal cancer.
铁氧化还原蛋白还原酶（FDXR）可能通过产生氧化应激，在5-氟尿嘧啶化疗介导的TP53凋亡中发挥作用。本研究采用TaqMan实时定量逆转录聚合酶链反应，发现51例结直肠癌患者肿瘤组织（中位数为212.9单位）和正常组织（中位数为113.8单位）之间FDXR相对RNA表达水平存在显著差异（P < 0.001）。在FDXR基因中发现了7个单核苷酸多态性（SNP），结肠肿瘤组织和正常组织之间的变异等位基因频率无显著差异（P > 0.05），并且结肠肿瘤样本和正常样本之间FDXR的常见单倍型没有差异。未观察到FDXR基因型与RNA表达之间的相关性，这意味着本研究中描述的多态性不调节结肠癌中FDXR的表达。这种基因组特征为FDXR对结直肠癌化疗影响的药物遗传学分析奠定了基础。
