2014
DOI: 10.1038/onc.2014.261
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Glioblastomas (GBMs) are resistant to current therapy protocols and identification of molecules that target these tumors is crucial. Interaction of secreted heat-shock protein 70 (Hsp70)-Hsp90-organizing protein (HOP) with cellular prion protein (PrP(C)) triggers a large number of trophic effects in the nervous system. We found that both PrP(C) and HOP are highly expressed in human GBM samples relative to non-tumoral tissue or astrocytoma grades I-III. High levels of PrP(C) and HOP were associated with greater… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
4
1

Citation Types

4
52
0

Year Published

2016
2016
2023
2023

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 47 publications
(56 citation statements)
references
References 53 publications
(69 reference statements)
4
52
0
Order By: Relevance
“…U87 cells were infected with lentiviral particles carrying two constructions targeted to the human PrP C sequence [15]. Efficiency was low for shRNA-PrP1 and high for shRNA-PrP2.…”
Section: Methodsmentioning
confidence: 99%
See 2 more Smart Citations
“…U87 cells were infected with lentiviral particles carrying two constructions targeted to the human PrP C sequence [15]. Efficiency was low for shRNA-PrP1 and high for shRNA-PrP2.…”
Section: Methodsmentioning
confidence: 99%
“…Erlich et al [16] reported that the interaction of PrP C with HOP modulates proliferation in glioma cell lines, and data from our group showed that higher expression of both proteins is correlated with greater tumor proliferation and lower survival in patients with GBM [15]. In addition, blocking the HOP-PrP C complex decreases tumor growth and increases survival in an animal model [15], making it a potential target for GBM therapy.…”
Section: Introductionmentioning
confidence: 96%
See 1 more Smart Citation
“…Interestingly, more recent studies suggested that PrP C plays a role in pluripotency and differentiation of embryonic stem cells [22], cell proliferation and differentiation [2328], and muscle cell regeneration [29], through the direct activation of the Src-family kinase Fyn, at least as far as the CNS effects [30]. Starting from these observations PrP C has been intriguingly involved in the development of human tumors [22, 31], including glioblastoma [32, 33], and gastric [34], breast [35], prostate [36], and colorectal [37] carcinomas. For example, PrP C expression was correlated with increased cell proliferation in gastric cancer cell lines [18, 38], and PrP C overexpression was shown to provide cancer cells with resistance to cytotoxic agents [36], and higher invasive properties [39].…”
Section: Introductionmentioning
confidence: 99%
“…Accordingly, glioblastomas, which are tumors derived from astrocyte precursors, also secrete STIP1 whose interaction with PRNP at the cell surface modulates the in vitro and in vivo proliferation of these tumor cells. 22 Remarkably, conditioned media from prnp-null astrocytes promote a reduced neuronal survival compared to media obtained from wild-type astrocytes. 19 Nonetheless, the role of PRNP in the secretion of trophic components, particularly those sorted to exosomes, is still unknown.…”
Section: Introductionmentioning
confidence: 99%