Abstract
BackgroundInvasion is a hallmark of a malignant tumor, such as a glioma, and the progression is followed by the interaction of tumor cells with an extracellular matrix (ECM). This study examined the role of type I collagen in the invasion of the malignant human glioma cell line T98G by the introduction of the human collagen type I α1 (HCOL1A1) gene.ResultsThe cells overexpressing HCOL1A1 were in a cluster, whereas the control cells were scattered. Overexpression of HCOL1A1 significantly suppressed the motility and invasion of the tumor cells. The glioma cell growth was markedly inhibited in vitro and in vivo by the overexpression of HCOL1A1; in particular, tumorigenicity completely regressed in nude mice. Furthermore, the HCOL1A1 gene induced apoptosis in glioma cells.ConclusionThese results indicate that HCOL1A1 have a suppressive biological function in glioma progression and that the introduction of HCOL1A1 provides the basis of a novel therapeutic approach for the treatment of malignant human glioma.
Highlights
Invasion is a hallmark of a malignant tumor, such as a glioma, and the progression is followed by the interaction of tumor cells with an extracellular matrix (ECM)
The processes of tumor cell invasion into the stromal tissue are closely related to the interactions between tumor cells and extracellular matrix (ECM)
Endostatin, a non-collagenous C-terminal domain (NC1) fragment of type XVIII collagen, was the first endogenous fragment characterized with anti-angiogenic properties [4]
Summary
Invasion is a hallmark of a malignant tumor, such as a glioma, and the progression is followed by the interaction of tumor cells with an extracellular matrix (ECM). This study examined the role of type I collagen in the invasion of the malignant human glioma cell line T98G by the introduction of the human collagen type I α1 (HCOL1A1) gene. The processes of tumor cell invasion into the stromal tissue are closely related to the interactions between tumor cells and extracellular matrix (ECM). Fragments of type IV, type XV, and type XVIII collagen, which are components of various basement membranes, have been extensively studied for their potential in the reduction of angiogenesis and tumorigenesis [2,3]. The NC1 fragments of type XV collagen and type IV collagen were identified as an endogenous angiogenesis inhibitor [5,6,7,8,9,10,11]
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