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| Expression and Clinical Significance of Metastasis-associated in Colon Cancer-1 and KAI1/CD82 in Hepatocellular Carcinoma |
| WANG Chun-rong |
| Department of Hepatobiliary Surgery, Xuanhan People's Hospital, Dazhou, Sichuan, 636150 |
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Abstract 【Objective】To explore the expression of MACC1 and KAI1/CD82 in hepatocellular carcinoma (HCC) patients , as well as the correlation with clinicopathological features. 【Methods】The expression levels of both MACC1 and KAI1/CD82 in 61 cases of HCC tissues and corresponding adjacent liver tissues were detected by immunohistochemistry, and the differences of MACC-1 and KAI1/CD82 protein expression between the two groups were compared. According to the clinical and pathological typing, the specimens of HCC radical resection group were grouped in order to reveal the difference of expression between the groups, and further explore the correlation between the expression of MACC-1 and KAI1/CD82 protein and clinical features. 【Results】Compared to adjacent tissues, MACC1 was significantly overexpressed in HCC tissues (P<0.05), while KAI1/CD82 was significantly down-expressed (P<0.05). The levels of MACC1 and KAI1/CD82 protein were correlated with tumor grade, lymph node metastasis, depth of invasion, and TNM stage (P<0.05). The overall survival time of patients with MACC1- or KAI1/CD82-positive HCC tumors was significantly longer than that of patients with MACC1 positive or KAI1 negative HCC (P<0.05). Importantly, multivariate analysis suggested that positive expression of either MACC1 or KAI1/CD82, as well as TNM stage, could be independent prognostic factors for overall survival in patients with HCC. 【Conclusion】 Abnormal expression of MACC1 and KAI1/CD82 plays an important role in the development of HCC. The combined detection of MACC1 and KAI1/CD82 is a biomarker for potential differential diagnosis of tumor metastasis and prognosis in HCC patients. MACC1 and KAI1/CD82 may represent promising metastatic and prognostic biomarkers, as well as potential therapeutic targets, for HCC.
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Received: 28 December 2018
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2019, Vol. 36 
