Long non‐coding RNA HULC stimulates the epithelial–mesenchymal transition process and vasculogenic mimicry in human glioblastoma

Abstract

Background

Long non‐coding RNA (lncRNA) HULC (highly upregulated in liver cancer) is considered as an oncogenic factor for various malignant tumors. This study aimed to reveal the role of lncRNA HULC in the malignant behavior of glioblastoma (GBM) by exploring its effects on the epithelial–mesenchymal transition (EMT) and vasculogenic mimicry (VM) of human GBM.

Materials and Methods

The contents of VM in 27 GBM samples were assessed by immunohistochemistry‐histology and their association with progress‐free survival (PFS) was analyzed. Human GBM SHG44 and U87 cells were manipulated to establish stable lncRNA HULC overexpressing and silencing cells by lentivirus‐based technology. The effects of altered lncRNA HULC on vasculogenic tubular formation, invasion, and EMT process in GBM cells were tested in vitro and the growth of implanted GBM tumors and their EMT process were examined in vivo.

Results

The numbers of VM were positively associated with disease progression, but negatively with PFS periods of GBM patients. Compared with the control vec cells, lncRNA HULC overexpression significantly increased the tubular formation, invasion, and EMT process of both SHG44 and U87 cells, accompanied by promoting the growth of implanted GBM tumors and EMT process in mice. LncRNA HULC silencing had opposite effects on the tubular formation, invasion, and EMT process as well as tumor growth of GBM cells.

Conclusion

LncRNA HULC stimulates the EMT process and VM in human GBM, and may be a therapeutic target for intervention of GBM.

Abstract

LncRNA HULC may increase VM to promote the progression of glioblastoma (GBM) by enhancing the epithelial–mesenchymal transition process in GBM. Our findings may uncover a therapeutic target and help in understanding the molecular pathogenesis of GBM.