Background: The mechanism of regulation of KAI1, a specific tumor metastasis suppression gene, is controversial. A recent study showed that the synergism of wild-type p53 and JunB has the function of regulating the expression of KAI1, a metastasis inhibiting factor in prostate cancer cells. The wild-type p53 gene is an activator of apoptosis and is closely related to malignant tumor cell multiplication. JunB, a member of the fos/jun family, is a key component of activator protein transcription factor and a major target element in the transmission pathway of mitosis. This study aimed to evaluate the relationship between the expression of KAI1 and p53 combined with JunB in tumor tissues and clinical outcomes in hepatocellular carcinoma (HCC) patients.
Methods: Quantitative real-time RT-PCR, Western blotting techniques and immunohistochemistry were used to evaluate the expression of KAI1 mRNA, KAI1/CD82, p53 and JunB in HCC patients, and the relationship between their expression and the clinicopathological prognostic parameters was analyzed.
Results: In cancer tissues, the values for positive expression of KAI1 mRNA, KAI1/CD82, p53 and JunB were 31.25%, 26.25%, 48.75%, and 20.00%, respectively, while in adjacent non-tumor tissues, they were 100%, 94.74%, 2.63%, and 76.32%, respectively. There was no correlation between the expression levels of p53 or JunB and KAI1 mRNA or KAI1/CD82. However, there were significant correlations between the expression levels of p53 combined with JunB and not only KAI1 mRNA but also KAI1/CD82 proteins.
Conclusions: When p53 dysfunction and low expression of JunB are simultaneous, they may play an important role in down-regulating the expression of KAI1 by synergism in HCC. But further studies in vivo and in vitro are needed to verify these results.