| In 1974, Berezney and Coffey first described the nuclear matrix (NM) as the structural framework scaffolding of the nucleus,It can be separated from the rest of the nucleus by applying DNAase digestion followed by salt extraction. Virtually it is independent reminder sub-nuclear structure after being devoid of membrane lipid, soluble histone and chromatin. According to many investigations, nuclear matrix has been shown to play an important role not only in maintaining the structure of nucleus, but also in chromatin/chromosome construction and DNA replication,transcription,repair and RNA synthesis,splicing and transportation. Given that the nuclear matrix proteins (NMPs) play an important role in these vital cellular functions, then which could participate in the generation and development tumor. Recently many investigations show: Cell line is different, composition of its nuclear matrix protein is different too. Compairing to normal cells, tumor cells exist in specific nuclear matrix proteins. It is obviously nuclear matrix proteins are special to tissues and cells. Separation and identification of tumor associated NMPs have been a new way to search for tumor specific markers and to study tumor pathogenesis. Nowadays several tumor specific NMPs have been separated and identified from hepatocellular cancer, colon cancer, prostate cancer and breast cancer, etc. Some of them (such as NMP22 NMP66) have been applied to clinical diagnosis and therapy, but studies of the separation and identification and specific markers of esophageal cancer the specific NMPs may have not been founded. P16 gene low-expression exists in many tumour tissues.Certainly,including esophageal cancer. When P16 gene only combines with nuclear matrix proteins, it can plays an important role in tissues. The correlation between the nuclear matrix proteins in esophageal cancer and the p16 gene, especially the upstream of p16 gene has not yet been reported.Objective: To study the association between the nuclear matrix proteins in esophageal cancer and the upstream of p16 gene, aimed at discussing the pathogenesis of esophageal cancer. Methods: the plasmid translation, the objective DNA callback,the DNA probe preparation,SDS-PAGE technique and southwestern blot are applied to study the nuclear matrix proteins of 24 cases of esophageal cancer,adjacent cancer tissue(adjacent cancer tissue is depart from cancer> 3.0cm) and normal esophageal tissues. UVPtool software is used to carry through quantitative analysis. Result: SDS-PAGE showed that the expressional quantity of 28kD nuclear matrix proteins in esophageal cancer tissues was decreased significantly compared with that in the normal esophageal tissues (P < 0. 05). Southwestern blot shows 28kD, 30kD, 40kD, 43kD proteins in normal tissues, and 50kD~66kD proteins in cancer tissues. The positive signal of 54kD protein binding to the upstream of p16 gene in cancer tissues was significantly higher than that in normal tissues. There was no significant difference between the various differentiated types and between the various clinical stages of esophageal cancer tissues. Conclusion: The alteration of nuclear matrix proteins and the binding of 54kD protein to the upstream of p16 gene in esophageal cancer might be relative in the development of esophageal cancer. |