Background & objective: Studies showed that the abnormal expression of atypical protein kinase C iota subtype (aPKC-iota) and E-cadherin plays an important role in tumor genesis and progression. This study was to investigate the expression of aPKC-iota and E-cadherin in cholangiocarcinoma, and analyze molecular mechanisms of the invasion and metastasis of cholangiocarcinoma.
Methods: The expression of aPKC-iota and E-cadherin in 9 specimens of benign bile duct tissues and 35 specimens of cholangiocarcinoma was detected by EnVision immunohistochemistry, and their correlations to the clinicopathologic characteristics and invasion of cholangiocarcinoma were analyzed.
Results: The positive rate of aPKC-iota was significantly higher in cholangiocarcinoma than in benign bile duct tissues (68.6% vs. 11.1%, P = 0.006), while the positive rate of E-cadherin was significantly lower in cholangiocarcinoma than in benign bile duct tissues (37.1% vs. 88.9%, P = 0.016). aPKC-iota expression was negatively correlated to E-cadherin expression (r = -0.287, P < 0.05). aPKC-iota expression was positively and E-cadherin expression was negatively correlated to the differentiation and invasion of cholangiocarcinoma (P < 0.05).
Conclusions: The expression of aPKC-iota and E-cadherin may reflect the differentiation and invasive potential of cholangiocarcinoma. As a polar regulation-associated protein, aPKC-iota may play a role in the invasion and metastasis of cholangiocarcinoma.