Correlation Research Between TAM And Gastric Cancer Cell EMT

BACKGROUND:Gastric cancer is one of the most common malignant tumors in the world. Although its overall incidence around the world is declining, the new cases of gastric cancer still account for9%of all the malignancies, according to statics in2005, right behind lung cancer, mammary cancer and colorectal cancer. Invasion, metastasis and recurrence are the major causes of gastric cancer patients'death and the key factors affecting clinical treatment and prognosis. The ability of malignant tumor cells to detach themselves from the primary tumor and invade adjacent, healthy tissue is the prerequisite for the subsequent development of distant metastases. Growing evidence suggests that the change in tumor tissue architecture takes place through a peculiar phenotype modulation known as EMT. EMT is a process by which epithelial cells modulate their phenotype and acquire mesenchymal-like properties through the disruption of intercellular adhesion and the enhancement of cell motility. Many epithelial tumors undergo an EMT that facilitates their invasion. Moreover, the stroma is an active participant in tumor progression, with complex interactions between tumor and stromal cells. Macrophages form a major component of the inflammatory infiltration and are termed TAM. Compelling evidence has emerged in recent years for TAM playing an important role in tumor cell invasion into surrounding normal tissues, proliferation and survival, and metastasis to local and distant sites. High levels of TAM are often correlated with a bad prognosis. TAMs facilitate angiogenesis, extracellular matrix breakdown, and tissue remodeling, and thus promote tumor cell motility. But their effects on tumor cells are not well understood. It is reported that there was a positive correlation between TAM and EMT in mammary cancer and lung cancer. However, whether TAM promote tumor invasion through inducing EMT is still unclear and need further investigation.OBJECTIVE:To investigate the correlation between TAM and EMT in gastric cancer tissues and the clinical significance.METHODS:1. The expression of E-cadrerin and CD68in120specimens of gastric cancer tissues and120specimens of adjacent gastric mucosa tissues was detected by immunohistochemistry (IHC). Analyze the differences between gastric cancer tissues and adjacent tissues.2. The relationship between their expression and clinicopathological features was statistically analyzed.3. Analyze the correlation between E-cadrerin and CD68expression in gastric cancer tissues.RESULTS:1. Compared to adjacent gastric mucosa tissues, the expression of E-cadherin in gastric cancer tissues was lower, while CD68was significantly higher (P<0.05). 2. The expression of E-cadherin was statistically significantly associated with depth of invasion, histologic type, TNM stage and numbers of lymph node metastasis (P<0.05); the expression of CD68was statistically significantly associated with the size of tumor, depth of invasion, TNM stage and numbers of lymph node metastasis (P<0.05).3. There was significant negative correlation between E-cadherin and CD68expression in gastric cancer tissues (r=-0.310, P<0.05).CONCLUSION:1. The expression of E-cadherin in gastric cancer tissues was low and was associated with depth of invasion, histologic type, TNM stage and numbers of lymph node metastasis.2. Infiltrating TAMs in gastric cancer tissues was statistically significantly associated with the size of tumor, depth of invasion, TNM stage and numbers of lymph node metastasis closely related to the aggression of gastric cancer.3. There was significant negative correlation between E-cadherin and CD68expression in gastric cancer tissues.