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: EC:3.4.22.62 (
caspase-9
)
7,507
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Overexpression of
Tafazzin
(
TAZ
), a mitochondrial protein, is often observed in many cancers. However, the association between aberrant expression of
TAZ
and drug resistance remains unclear. The aim of this study is to explore the role of
TAZ
in regulating the TRAIL resistance in glioma. We thus established the TRAIL resistance models on glioma by using the U87 and U251 cell lines (U87/R and U251/R). As the results, obvious overexpression of
TAZ
was observed in U87/R and U251/R cells. However, knockdown of
TAZ
increased the sensitivity of U87/R and U251/R cells to TRAIL-induced apoptosis. By contrast, expression of miR-125b was downregulated in U87/R and U251/R cells compared to the parental U87 and U251 cells. Furthermore, decrease of miR-125b was responsible for overexpression of
TAZ
, because the results of dual-luciferase reporter assays verified that
TAZ
was targeted by miR-125b. We then showed that enforced expression of miR-125b resensitized the U87/R and U251/R cells to TRAIL-dependent damage of mitochondria and activation of
caspase-9
and -3. We demonstrated that overexpression of
TAZ
caused by downregulation of miR-125b promoted resistance of glioma cells to TRAIL. MiR-125b/
TAZ
axis may represent a potential strategy to reverse the TRAIL in glioma.
...
PMID:Downregulation of miR-125b promotes resistance of glioma cells to TRAIL through overexpression of Tafazzin which is a mitochondrial protein. 3105 33
