Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0017638 (
glioma
)
30,880
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Objective:
Temozolomide (TMZ) is commonly used for glioblastoma multiforme (GBM) chemotherapy. However, drug resistance limits its therapeutic effect in GBM treatment. RNA-binding proteins (RBPs) have vital roles in posttranscriptional events. While disturbance of RBP-RNA network activity is potentially associated with cancer development, the precise mechanisms are not fully known. The
SNRPG
gene, encoding
small nuclear ribonucleoprotein polypeptide G
, was recently found to be related to cancer incidence, but its exact function has yet to be elucidated.
Methods:
SNRPG
knockdown was achieved via short hairpin RNAs. Gene expression profiling and Western blot analyses were used to identify potential
glioma
cell growth signaling pathways affected by
SNRPG
. Xenograft tumors were examined to determine the carcinogenic effects of
SNRPG
on
glioma
tissues.
Results:
The
SNRPG
-mediated inhibitory effect on
glioma
cells might be due to the targeted prevention of Myc and p53. In addition, the effects of
SNRPG
loss on p53 levels and cell cycle progression were found to be Myc-dependent. Furthermore,
SNRPG
was increased in TMZ-resistant GBM cells, and downregulation of
SNRPG
potentially sensitized resistant cells to TMZ, suggesting that
SNRPG
deficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling pathway. Our data confirmed that
SNRPG
suppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling cascade.
Conclusions:
These results indicated that
SNRPG
is a probable molecular target of GBM and suggested that suppressing
SNRPG
in resistant GBM cells might be a substantially beneficial method for overcoming essential drug resistance.
...
PMID:Downregulation of SNRPG induces cell cycle arrest and sensitizes human glioblastoma cells to temozolomide by targeting Myc through a p53-dependent signaling pathway. 3229 80