Epithelial–mesenchymal transition (EMT) is known to promote HCC cell migration, invasion, and metastasis. The concrete mechanisms of HCC pathogenesis are not fully understood. These two factors make long-term prognosis poor for HCC patients. Moreover, lung metastasis occurs in many HCC patients with advanced disease. Due to the lack of significant symptoms and signs at an early stage of the disease, more than 50% of patients with HCC are first diagnosed at an advanced tumor stage. The global incidence of hepatocellular carcinoma (HCC) is rising worldwide. Lnc-Ma301 may help regulate onset and metastasis of HCC. Mechanistic studies suggested that lnc-Ma301 interacts with caprin-1 to inhibit HCC metastasis and EMT through Akt/Erk1 pathway. Activation of lnc-Ma301 inhibited cell proliferation, migration and EMT in HCC cell cultures, and it inhibited lung metastasis of HCC tumors in mice. Lnc-Ma301 showed lower expression in HCC tissues than in adjacent normal tissues, and lower expression was associated with worse prognosis. Microarray analyses identified lnc-Ma301 as one of the most overexpressed long non-coding RNAs during polarization of U937 macrophages from M2 to M1 phenotype. Effects of lnc-Ma301 over- and underexpression on the Akt/Erk1 signaling pathways were examined. Interactions among lnc-Ma301 and its potential downstream targets caprin-1 were investigated in HCC cell lines. lnc-Ma301 was overexpressed or knocked-down in HCC cell lines, and the effects were assessed in vitro and in vivo. The expression of the identified lncRNA was compared between clinical samples of HCC tissues or adjacent normal tissues, as well as between HCC and normal liver cell lines. Microarray analysis was used to identify lncRNAs expression during polarization of U937 macrophages from M2 to M1 phenotype. The molecular mechanisms behind EMT and metastasis in HCC remain unclear. Epithelial–mesenchymal transition (EMT) promotes migration, invasion, and metastasis of hepatocellular carcinoma (HCC) cells.
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