2019
DOI: 10.1007/s00109-019-01843-4
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Co-delivery of GOLPH3 siRNA and gefitinib by cationic lipid-PLGA nanoparticles improves EGFR-targeted therapy for glioma

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Cited by 32 publications
(32 citation statements)
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“…The action of gefitinib was also investigated by Wang and collaborators, who found that both immortalized and primary glioma cells with higher GOLPH3 levels also display a higher sensitivity to gefitinib [75]. These data partly contrast with the findings of Ye and collaborators [74], described above, on the GOLPH3 levels that are coupled with the gefitinib-based therapeutic strategy. Finally, Peng and co-workers [76] demonstrated that GOLPH3 is also a direct target of miR-299-5p in GBM cell lines (T98G and A172); moreover, miR-299-5p knockdown makes GBM cells sensitive to temozolomide (TMZ) both in vitro and in vivo by impairing cell proliferation and invasion and promoting apoptosis through the inhibition of the ERK signaling pathway.…”
Section: Golph3 Deregulation and Brain Tumorsmentioning
confidence: 94%
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“…The action of gefitinib was also investigated by Wang and collaborators, who found that both immortalized and primary glioma cells with higher GOLPH3 levels also display a higher sensitivity to gefitinib [75]. These data partly contrast with the findings of Ye and collaborators [74], described above, on the GOLPH3 levels that are coupled with the gefitinib-based therapeutic strategy. Finally, Peng and co-workers [76] demonstrated that GOLPH3 is also a direct target of miR-299-5p in GBM cell lines (T98G and A172); moreover, miR-299-5p knockdown makes GBM cells sensitive to temozolomide (TMZ) both in vitro and in vivo by impairing cell proliferation and invasion and promoting apoptosis through the inhibition of the ERK signaling pathway.…”
Section: Golph3 Deregulation and Brain Tumorsmentioning
confidence: 94%
“…Yuan and collaborators [73] targeted GOLPH3 through siRNA loaded on cationic liposomes, obtaining the inhibition of glioma growth in vivo, in a nude mouse model. A similar nanoparticle-mediated approach was used by Ye and co-workers, who co-delivered GOLPH3 siRNA and gefitinib (Ge, an anti-EGFR drug) in vitro (U87 and T98G glioma cell lines) and in vivo (BALB/c nude mice), obtaining growth inhibition and apoptosis induction [74]. The action of gefitinib was also investigated by Wang and collaborators, who found that both immortalized and primary glioma cells with higher GOLPH3 levels also display a higher sensitivity to gefitinib [75].…”
Section: Golph3 Deregulation and Brain Tumorsmentioning
confidence: 99%
“…They demonstrated that Angiopep-2modified cationic lipid polymer crosses the BBB. Gefitinib can inhibit EGFR signaling and block the autophosphorylation of critical tyrosine residues on EGFR whereas GOLPH3 siRNA downregulate GLOPH3 expression (Ye et al, 2019).…”
Section: Tumormentioning
confidence: 99%
“…43) Therefore, the ApoE protein or ApoE-derived peptide modification approach targeting LDLR was developed. [44][45][46] LDLR family-targeting peptides, such as Angiopep-2 [47][48][49] or Peptide-22 50,51) were also developed. Chen et al evaluated the BBB-targeting ability of liposomes modified with various BBB-targeting (Angiopep-2, T7, Peptide-22) and gliomatargeting (c(RGDfK), D-SP5, peptide-1) ligands.…”
Section: Formulationmentioning
confidence: 99%
“…105) However, Tamaru et al developed plasmid DNA-encapsulated liposomal nanoparticles with a neutral charge and they succeeded in efficient transfection in the SVZ. 46) Recently, external stimuli have been used to deliver transfected genes via ICV administration. Bugeon et al genetically manipulated NSCs and neuronal cells in the SVZ by ICV injection of mRNA followed by electroporation.…”
Section: Intraventricular Administrationmentioning
confidence: 99%