| Pancreatic carcinoma is a kind of most malignant tumor and its survival rate is less than 5% in 5 years. Till now, the main therapeutic method for pancreatic carcinoma is surgical operation. Although binding with chemical therapy and radiotherapy, the result is not satisfactory. The tumorgenesis and development of pancreatic carcinoma has been generally accepted as a complex multi-step process involving multi-genetic changes. And gene therapies have been taken according to some genes in previous researches. But there has not been a clear breakthrough. Recently, the new developed technologies, such as genome chip, tissue array and proteomic technique have been used in researches of diseases. All of these will make great sense to elucidate the relationship between the genetic changes and human diseases, illuminate the mechanism of tumorgenesis and development and find out new therapy targets.FXYD3 was found by Microarray-based research assay. It is one of the highly differentially expressed genes in pancreatic cancer, chronic pancreatitis and normal pancreatic tissue. FXYD3 is one member of the FXYD protein family. It is also auxiliary subunit of Na-K-ATPase and regulates Na-K-ATPase activity in a tissue- and isoform-specific way. In normal tissue, FXYD3 is mainly expressed in the uterus, stomach, colon and skin. It has been found present in primary human breast carcinomas, human breast carcinoma cell lines, colorectal cancer cell lines and prostate carcinoma. FXYD3 is not only highly upregulated in specific types of cancers, such as breast or prostate tumors, but also has relationship with tumor staging. Although much has learned about the functional effects of FXYD3 on Na-K-ATPase, we are far from understanding the...
|
PDF Full Text Request