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:C0476089 (
endometrial cancer
)
11,379
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We previously reported frequent loss of
TESTIN
in human
endometrial carcinoma
, which significantly suppressed tumor proliferation and invasion. Herein, we further explored the mechanisms underlying
TESTIN
loss and its roles in the epithelial-mesenchymal transition (EMT, a key step for tumor spreading). Methylation-specific PCR was performed to investigate the promoter status of
TESTIN
in a panel of
endometrial cancer
and normal endometrium tissues. The expression of
TESTIN
mRNA was determined by real-time PCR. Up- and down-regulation of
TESTIN
were achieved by transient transfection with pcDNA3.1-
TESTIN
and shRNA-
TESTIN
plasmids, respectively. The EMT alterations were observed under the optical microscope and EMT-related markers were detected by real-time PCR and western blot. Compared to the control (3.6%),
TESTIN
was hypermethylated in 43.7%
endometrial cancer
tissues (p < 0.001). Moreover,
TESTIN
hypermethylation was significantly correlated with advanced tumor stage, deep myometrial invasion and lymphatic node metastasis. In vitro, the demethylating agent dramatically restored the expression of
TESTIN
. In addition, up-regulation of
TESTIN
significantly suppressed the EMT procedure; whereas down-regulation of
TESTIN
enhanced EMT. In conclusion, we demonstrated that loss of
TESTIN
was mainly caused by hypermethylation, which might be a potent prognostic marker. Furthermore, we proved that
TESTIN
significantly suppressed the EMT procedure, proposing restoration of
TESTIN
to be a novel therapeutic strategy for
endometrial carcinoma
.
...
PMID:TESTIN was commonly hypermethylated and involved in the epithelial-mesenchymal transition of endometrial cancer. 2572 Mar 71
