TY - JOUR
T1 - Suppression of peroxiredoxin 4 in glioblastoma cells increases apoptosis and reduces tumor growth
AU - Kim, Tae Hyong
AU - Song, Jieun
AU - Alcantara Llaguno, Sheila R.
AU - Murnan, Eric
AU - Liyanarachchi, Sandya
AU - Palanichamy, Kamalakannan
AU - Yi, Ji Yeun
AU - Viapiano, Mariano Sebastian
AU - Nakano, Ichiro
AU - Yoon, Sung Ok
AU - Wu, Hong
AU - Parada, Luis F.
AU - Kwon, Chang Hyuk
PY - 2012/8/15
Y1 - 2012/8/15
N2 - Glioblastoma multiforme (GBM), the most common and aggressive primary brain malignancy, is incurable despite the best combination of current cancer therapies. For the development of more effective therapies, discovery of novel candidate tumor drivers is urgently needed. Here, we report that peroxiredoxin 4 (PRDX4) is a putative tumor driver. PRDX4 levels were highly increased in a majority of human GBMs as well as in a mouse model of GBM. Reducing PRDX4 expression significantly decreased GBM cell growth and radiation resistance in vitro with increased levels of ROS, DNA damage, and apoptosis. In a syngenic orthotopic transplantation model, Prdx4 knockdown limited GBM infiltration and significantly prolonged mouse survival. These data suggest that PRDX4 can be a novel target for GBM therapies in the future.
AB - Glioblastoma multiforme (GBM), the most common and aggressive primary brain malignancy, is incurable despite the best combination of current cancer therapies. For the development of more effective therapies, discovery of novel candidate tumor drivers is urgently needed. Here, we report that peroxiredoxin 4 (PRDX4) is a putative tumor driver. PRDX4 levels were highly increased in a majority of human GBMs as well as in a mouse model of GBM. Reducing PRDX4 expression significantly decreased GBM cell growth and radiation resistance in vitro with increased levels of ROS, DNA damage, and apoptosis. In a syngenic orthotopic transplantation model, Prdx4 knockdown limited GBM infiltration and significantly prolonged mouse survival. These data suggest that PRDX4 can be a novel target for GBM therapies in the future.
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U2 - 10.1371/journal.pone.0042818
DO - 10.1371/journal.pone.0042818
M3 - Article
C2 - 22916164
AN - SCOPUS:84865054581
SN - 1932-6203
VL - 7
JO - PLoS One
JF - PLoS One
IS - 8
M1 - e42818
ER -