Abstract
BackgroundEpithelial–mesenchymal transition (EMT) promotes migration, invasion, and metastasis of hepatocellular carcinoma (HCC) cells. The molecular mechanisms behind EMT and metastasis in HCC remain unclear.MethodsMicroarray analysis was used to identify lncRNAs expression during polarization of U937 macrophages from M2 to M1 phenotype. 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. lnc-Ma301 was overexpressed or knocked-down in HCC cell lines, and the effects were assessed in vitro and in vivo. Interactions among lnc-Ma301 and its potential downstream targets caprin-1 were investigated in HCC cell lines. Effects of lnc-Ma301 over- and underexpression on the Akt/Erk1 signaling pathways were examined.ResultsMicroarray analyses identified lnc-Ma301 as one of the most overexpressed long non-coding RNAs during polarization of U937 macrophages from M2 to M1 phenotype. Lnc-Ma301 showed lower expression in HCC tissues than in adjacent normal tissues, and lower expression was associated with worse prognosis. Activation of lnc-Ma301 inhibited cell proliferation, migration and EMT in HCC cell cultures, and it inhibited lung metastasis of HCC tumors in mice. Mechanistic studies suggested that lnc-Ma301 interacts with caprin-1 to inhibit HCC metastasis and EMT through Akt/Erk1 pathway.ConclusionsLnc-Ma301 may help regulate onset and metastasis of HCC.
Highlights
The global incidence of hepatocellular carcinoma (HCC) is rising worldwide [1]
Microarray analysis of Long non-coding RNAs (lncRNAs) and mRNA during polarization from M2 to M1 cells At first, immunohistochemical staining was performed based on 30 paired HCC tissues and adjacent normal tissues
We found that the expression of CD163 was significantly higher in HCC tissues than in the adjacent tissues
Summary
The global incidence of hepatocellular carcinoma (HCC) is rising worldwide [1]. Due to the lack of significant symptoms and signs at an early stage of the disease, Luo et al Cancer Cell Int (2021) 21:422 induce HCC metastasis [5, 6]. The molecular details about how EMT is induced in HCC and how it may drive metastasis remain unclear. Tumor-associated macrophages (TAMs) mainly present the M2 phenotype and have important roles in both tumor progression and therapeutic response (including HCC) [9,10,11]. Epithelial–mesenchymal transition (EMT) promotes migration, invasion, and metastasis of hepatocel‐ lular carcinoma (HCC) cells. The molecular mechanisms behind EMT and metastasis in HCC remain unclear
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