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)
Although patients with glioblastoma (GBM) have grave prognosis, significant variability in patient outcome is observed. This study aims to identify novel targets for GBM diagnosis and therapy. Microarray data (GSE4290, GSE7696, and GSE4412) obtained from the Gene Expression Omnibus was used to identify the differentially expressed genes (DEGs) by significant analysis of microarray (SAM). Intersection of the identified DEGs for each profile revealed 46 DEGs in GBM. A subset of common DEGs were validated by real-time reverse transcription quantitative PCR (qPCR). The prognostic value of some of the markers was also studied. We determined that RRM2 and COL3A1 were increased and directly correlated with
glioma
grade, while
SH3GL2
and SNAP91 were decreased in GBM and inversely correlated with
glioma
grade. Kaplan-Meir analysis of GSE7696 revealed that COL3A1 and SNAP91 correlated with survival, suggesting that COL3A1 and SNAP91 may be suitable biomarkers for diagnostic or therapeutic strategies for GBM.
...
PMID:COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value. 2765 37
SH3GL2
(Src homology 3 (SH3) domain GRB2-like 2) is mainly expressed in the central nervous system and regarded as a tumour suppressor in human
glioma
. However, the molecular mechanism of the SH3GL2 protein involved in malignant behaviours of human
glioma
has not been elucidated. In this study, we tried to investigate the role of
SH3GL2
in
glioma
cell migration and invasion and explore its underlined molecular mechanism. Firstly, we discovered that the protein level of
SH3GL2
was widely decreased in the human
glioma
patients, especially in high-grade
glioma
tissues. Then, we determined the role of
SH3GL2
in migration and invasion of
glioma
cells upon
SH3GL2
knocking down and overexpressing. It was showed that knocking down of
SH3GL2
promoted the migration and invasion of
glioma
cells, whereas overexpression of
SH3GL2
inhibited them. Further study on molecular mechanism disclosed that silencing of
SH3GL2
obviously activated the STAT3 (signal transducer and activator of transcription 3) signalling thereby promoting the expression and secretion of MMP2. On the contrary, overexpression of
SH3GL2
had opposite effect. Taken together, the above results suggest that
SH3GL2
suppresses migration and invasion behaviours of
glioma
cells through negatively regulating STAT3/MMP2 signalling and that loss of
SH3GL2
may intensify the STAT3/MMP2 signalling thereby contributing to the migration and invasion of
glioma
cells.
...
PMID:Loss of SH3GL2 promotes the migration and invasion behaviours of glioblastoma cells through activating the STAT3/MMP2 signalling. 2847 Sep 49
