Overall, VCAN fragments promote tumorigenesis and inflammation, however, the specific cleavage site, the extent of cleavage activity, and the microenvironment in which cleavage occurs, collectively determine how this pleiotropic molecule and its fragments influence cells.
Twenty-four hub genes were confirmed, the survival analyses from the cBioPortal online platform revealed that topoisomerase (DNA) II α (TOP2A), periostin (POSTN), plasminogen activator, urokinase (PLAU), and versican (VCAN) may be involved in the carcinogenesis and progression of Pa, and the receiver-operating characteristic curves indicated their diagnostic value for Pa.
These results demonstrate that VCAN promotes ccRCC tumorigenesis and metastasis and thus is an attractive target for novel diagnostic, prognostic, and therapeutic strategies.<b>Implications:</b> This study highlights the oncogenic role of VCAN in renal cell carcinogenesis and suggests that this gene has therapeutic and/or biomarker potential for renal cell cancer.<i></i>.
The stromal alterations of versican and LTBP-4 might influence the carcinogenesis and progression of breast tumor cells and modulate their biological phenotypes.
Here, we report that astrocytoma U87 cells expressing the versican G3 mutant lost the hallmark of cell transformation and tumorigenesis in vitro and in vivo.