Proteomic profiling of fetal esophageal epithelium, esophageal cancer, and tumor-adjacent esophageal epithelium and immunohistochemical characterization of a representative differential protein, PRX6

Abstract

AIMTo understand the molecular mechanism of esophageal cancer development and provide molecular markers for screening high-risk populations and early diagnosis.METHODSTwo-dimensional electrophoresis combined with mass spectrometry were adopted to screen differentially expressed proteins in nine cases of fetal esophageal epithelium, eight cases of esophageal cancer, and eight cases of tumor-adjacent normal esophageal epithelium collected from fetuses of different gestational age, or esophageal cancer patients from a high-risk area of esophageal cancer in China. Immunohistochemistry (avidin-biotin-horseradish peroxidase complex method) was used to detect the expression of peroxiredoxin (PRX)6 in 91 cases of esophageal cancer, tumor-adjacent normal esophageal tissue, basal cell hyperplasia, dysplasia, and carcinoma in situ, as well as 65 cases of esophageal epithelium from fetuses at a gestational age of 3-9 mo.RESULTSAfter peptide mass fingerprint analysis and search of protein databases, 21 differential proteins were identified; some of which represent a protein isoform. Varying degrees of expression of PRX6 protein, which was localized mainly in the cytoplasm, were detected in adult and fetal normal esophageal tissues, precancerous lesions, and esophageal cancer. With the progression of esophageal lesions, PRX6 protein expression showed a declining trend (P < 0.05). In fetal epithelium from fetuses at gestational age 3-6 mo, PRX6 protein expression showed a declining trend with age (P < 0.05). PRX6 protein expression was significantly higher in well-differentiated esophageal cancer tissues than in poorly differentiated esophageal cancer tissues (P < 0.05).CONCLUSIONDevelopment and progression of esophageal cancer result from interactions of genetic changes (accumulation or superposition). PRX6 protein is associated with fetal esophageal development and cancer differentiation.

Redox Paradox: A Novel Approach to Therapeutics-Resistant Cancer

“…A high level of ROS from radiation could induce MnSOD and Prx6 expression as an adaptive response to protect radiation-mediated oxidative stress insult. In addition, increases of MnSOD and Prx6 have been associated with biochemical recurrence in prostate cancer patients after radical prostatectomy (275) as well as with fetal esophageal development (124,257). Thus, these two APs could be used as markers for the radioresistant phenotype in cancers.…”

Stemness specificity of epithelial cells – application of cell and tissue technology in regenerative medicine

“…The outermost layer of skin is composed of dead stratified squamous and keratinized epithelial cells [11]. Tissues that line the inside of the mouth, the oesophagus, the vagina, and part of the rectum are composed of the nonkeratinized stratified squamous epithelium [12][13][14]. Other surfaces that separate body cavities from the outside environment are lined by simple squamous, columnar, or pseudostratified epithelial cells.…”

Effects of Peroxiredoxin 6 and Its Mutants on the Isoproterenol Induced Myocardial Injury in H9C2 Cells and Rats

“…PRDX6 is the only1-Cys member with gonad-stimulating hormone (GSH) as electron donor in PRDX family, with dual enzyme activities of both glutathione peroxidase (GPX) and phospholipase A2 (PLA2), and its main function in the body is to regulate redox reaction and phospholipid metabolism [ 10 ]. Moreover, PRDX6 plays an important protection role in the pathological state of different oxidative injuries of skin, lung, eyes, gastrointestinal tract, nervous system, and ovary [ 11 – 13 ]. However, the role of PRDX6 in myocardial ischemia is still unclear.…”