Abstract
Aim. To detect the expression of dual oxidase (DUOX) 2 in Barrett esophagus, gastric cancer, and colorectal cancer (CRC). Materials and Methods. The endoscopic biopsies were collected from patients with Barrett esophagus, while the curative resection tissues were obtained from patients with gastric cancer, CRC, or hepatic carcinoma. The DUOX2 protein and mRNA levels were detected with immunohistochemistry (IHC) and real-time quantitative PCR (qPCR). The correlation of DUOX2 expression with clinicopathological parameters of tumors was identified. Results. Low levels of DUOX2 mRNA were detected in Barrett esophagus and the adjacent normal tissues, and there was no difference between these two groups. DUOX2 protein was found in Barrett esophagus and undetectable in the normal epithelium. The DUOX2 mRNA and protein levels in the gastric cancer and CRC were increased compared to the adjacent nonmalignant tissues. The elevated DUOX2 in the gastric cancer was significantly associated with smoking history. In CRC tissues, the DUOX2 protein expression level in stages II–IV was significantly higher than that in stage I. In both hepatic carcinoma and the adjacent nonmalignant tissue, the DUOX2 was virtually undetectable. Conclusion. DUOX2 in Barrett esophagus, gastric cancer, and CRC may be involved in the tumorigenesis of these tissues.
Highlights
Reactive oxygen species (ROS) are oxygen-derived small molecules, including hydrogen peroxide (H2O2), hydroxyl radical, singlet oxygen, and superoxide [1]
DUOX2 mRNA was expressed at low levels in adjacent nontumorous tissues, the DOUX2 mRNA in gastric cancer was increased 3.9-fold compared to adjacent nonmalignant control
Our results show the presence of DUOX2 protein in Barrett esophagus but not in normal esophagus suggesting that DUOX2 may be involved in the carcinogenesis process of Barrett esophagus via ROS production
Summary
Reactive oxygen species (ROS) are oxygen-derived small molecules, including hydrogen peroxide (H2O2), hydroxyl radical, singlet oxygen, and superoxide [1]. ROS serve as intrinsic signaling molecules and regulate normal physiological processes such as cardiac-vascular vessel contraction, immune defense, regulation of transcription, signal transduction, and hormone biosynthesis [2]. When ROS levels are either too low or too high, they cause alteration in cell function and structure. The low ROS levels are related to decreased antimicrobial defense and hypothyroidosis. The abundant ROS may react with proteins, lipids, carbohydrates, and nucleic acids, resulting in cell membrane damage, DNA base modifications, deoxyribose damage, and single- and double-stranded DNA breaks [3]. A large body of evidence shows that excessive ROS are involved in many types of disease process, including inflammation and cancer [4, 5]
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