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Abstract
BackgroundIncreasing amounts of evidence indicate that Missing in metastasis B (MIM-B) promotes cancer metastasis. Here, we sought to better understand the mechanism through which MIM-B promotes tumor metastasis in hepatocellular carcinoma (HCC).MethodsWe performed confocal microscopy analysis to determine the distributions of MIM-B and caveolin-1 and conducted co-immunoprecipitation assays to detect the interactions between MIM-B and caveolin-1 in vitro. We performed transwell assays to analyze the invasive ability of HCC cells. Changes in the expression levels of key genes and some molecular makers were detected by immunohistochemistry and western blotting in HCC tissue samples.ResultsWe found that MIM-B co-localizes with caveolin-1 and demonstrated that MIM-B and caveolin-1 interact in vitro. Repressing MIM-B and caveolin-1 expression inhibited the epidermal growth factor receptor signaling pathway. We overexpressed MIM-B and caveolin-1 in Hep3B cells, which enhanced Hep3B cell invasiveness. Furthermore, MHCC97H cell invasiveness was significantly decreased in cells in which MIM-B and caveolin-1 expression was inhibited. Additionally, we found that MIM-B and caveolin-1 were expressed at higher levels in HCC tissues than in paired normal tissues. Moreover, HCC patients with MIM-B and caveolin-1 up-regulation experienced significantly worse outcomes than controls (P < 0.001), and HCC patients with high MIM-B and caveolin-1 expression levels often developed pulmonary metastasis (P < 0.001).ConclusionsMIM-B combined with caveolin-1 promotes metastasis of HCC, and elevated MIM-B and caveolin-1 expression levels are associated with a poor prognosis in HCC patients; therefore, MIM-B and caveolin-1 may represent novel targets for the diagnosis and treatment of HCC.
Highlights
Primary liver cancer is one of most commonly diagnosed cancers and is one of the leading causes of cancer-related death worldwide
Missing in metastasis B (MIM-B) combined with caveolin-1 promotes metastasis of hepatocellular carcinoma (HCC), and elevated MIM-B and caveolin-1 expression levels are associated with a poor prognosis in HCC patients; MIM-B and caveolin-1 may represent novel targets for the diagnosis and treatment of HCC
Given that caveolin-1 is co-localized with MIM-B, we proposed that MIM-B interacted with caveolin-1
Summary
Primary liver cancer is one of most commonly diagnosed cancers and is one of the leading causes of cancer-related death worldwide. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and accounts for approximately 75% of liver tumors [1]. Hepatic resection is currently the most frequently used treatment for patients with HCC [2]. HCC is usually diagnosed at an advanced stage, which limits the effectiveness of this treatment. The rates of HCC recurrence and metastasis are very high at 5 years after surgery, even among patients who have undergone radical hepatic resection [3]. The post-resection biological features of HCC warrant further study. Increasing amounts of evidence indicate that Missing in metastasis B (MIM-B) promotes cancer metastasis. We sought to better understand the mechanism through which MIM-B promotes tumor metastasis in hepatocellular carcinoma (HCC)
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