| Ovarian cancer is one of the most common neoplasm for females and epithelial tumor of ovary accounts for 90% of this disease. The onset of ovarian cancer is secret and not easy to be detected, but easy to metastasis with bad prognosis. Its mobility only ranks after cervical cancer and corpus carcinoma, but its morbidity ranks the first, seriously threatening women lives. Copious knowledge has been accumulated through pathologic morphology, mechanism exploration and therapeutic regimen of ovaries researches. However, the five year survival rate is only 25-30% according to clinical data. Tight junction (TJ) abnormality is now considered to be the prerequisite for tumor metastasis owing to the special structure and function of tight junction.TJs are conjunction complex locating in epithelial and endothelial cells, making adjacent cells hugging together, forming a barricade around cells and enclosing intercellular space, playing a key role in maintaining cell polarity, permeability, mobility and regulation of cell proliferation and differentiation. They mainly consist of three necessary membrane proteins-claudins, occludins and JAM. Their expression modes differ largely in different tissues, and even in the same tissue the difference still exists. Recent researches suggest that the invasive and metastasis of ovarian cancer cells are associated with the abnormality of TJs structure and function through activating MMPs. The mechanism is still under investment.This research was conducted to investigate the relationship between ovarian cancer cell metastasis and TJs ,such as claudin-6,occludin and MMP-2, through protein expression detection in 36 cases ovarian cancer and 26 cases benign neoplasm by histoimmunochemistry. By analyzing the clinical the clinical indexes of clinical stage, pathological grading and metastasis, we explored the role that Claudin-6,Occludin and MMP-2 played in carcinogenesis, metastasis and invasion of ovarian cancer cells. The results showed as followings:1. Claudin-6 mainly expressed in cytoplasm and membrane of ovarian cancer cells. Claudin-6 was positive in 25 cases among 36 cases, with 69.44% positive rates. In benign neoplasm, Claudin-6 was positive in 9 cases among 26 cases, with 34.62 positive rates. Claudin-6 expression in malignant tumor is significantly higher than in benign neoplasm (P<0.05. The positive rate in metastasis group was higher than in no metastasis group even if no statistical significance was found between the two groups. But in a way, claudin-6 expression upregulation could be considered associating with tumor cell carcinogenesis and metastasis. No remarkable relationship was found among Claudin-6 expression, age, pathologic grading or clinical stage (p>0.05).2. In ovarian cancer tissues, Occludin expression was positive in 19 cases among 36 cases, with 52.78% positive rate; while in benign neoplasm, Occludin expression was found in 17 cases among 26 cases, with 56.38% positive rate. The difference was not significant between the two groups ( P>0.05 ) . No remarkable relationship was found among Occludin expression, age, pathologic grading or clinical stage (p>0.05).3. MMP-2 expression rate in ovarian cancer tissue was 72.22% and 30.77% in benign neoplasm. The difference was notable between the two groups (P<0.05). MMP-2 expression level in cancer group was remarkably higher in ovarian cancer tissue than in benign tissue (P<0.05) and increasing significantly with the progress of clinical stage. No significant relationship was found among MMP-2 expression, age, pathologic grading or clinical stage (p>0.05). MMP-2 can be used as a marker to judge ovarian cancer cell malignancy and metastasis.4. Correlation analysis of Claudin-6, Occludin and MMP-2 expression showed that no significantly relationship was found between any two groups(P>0.05).In summary, the above results show that the upregulation of Claudin-6 and MMP-2 plays a role in ovarian cancer carcinogenesis and metastasis by influencing TJs structure and function, and can be used as an index for the judgment of ovarian cancer carcinogenesis and metastasis.
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