These cells expressed high Cathepsin L levels, and when grown as monolayers and spheroids, they were more resistant to As<sub>2</sub>O<sub>3</sub> than the U87MG glioblastoma cell line.
Since p53 pathways are often mutated in glioblastoma, the findings of our study need to be considered before using cathepsin L inhibition for glioblastoma therapy and suggest that such adjuvant therapy may be effective only for a subpopulation of p53 wild type glioblastoma patients.
In view of its role in tumorigenesis, angiogenesis and tumor cell invasion, increased expression of cathepsin L in glioblastoma cells harboring wild type p53 might confer invasive ability and growth advantage to these cells.
These results prove for the first time that over-expression of VEGF in human glioblastoma cells induces cathepsin L expression at the transcriptional level.
These results prove for the first time that over-expression of VEGF in human glioblastoma cells induces cathepsin L expression at the transcriptional level.
Increased chemoresistance of tumour cells may be associated with increased levels of CatL and may have potential application in gene therapy, which would augment the apoptosis of glioblastoma cells induced by chemotherapy.