Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
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Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: UMLS:C1522282 (
EMT
)
2,868
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The proteins of the Inhibitor of Growth (ING) candidate tumor suppressor family are involved in multiple cellular functions such as cell cycle regulation, apoptosis, and chromatin remodeling. ING5 is the new member of the family whose actual role in tumor suppression is not known. Here we show that ING5 overexpression in lung cancer A549 cells inhibited cell proliferation and invasiveness, while ING5 knockdown in lung cancer H1299 cells promoted cell aggressiveness. ING5 overexpression also abrogated tumor growth and invasive abilities of lung cancer cells in mouse xenograft models. Further study showed that ING5 overexpression inhibited
EMT
indicated by increase of E-cadherin and decrease of N-cadherin, Snail and slug at mRNA and protein levels, which was accompanied with morphological changes. cDNA microarray and subsequent qRT-PCR validation revealed that ING5 significantly downregulated expression of
EMT
(epithelial to mesenchymal transition)-inducing genes including CEACAM6, BMP2 and
CDH11
. Clinical study by tissue microarray showed that nuclear ING5 negatively correlated with clinical stages and lymph node metastasis of lung cancer. Furthermore, high level of nuclear ING5 was associated with a better prognosis. Taken together, these findings uncover an important role for ING5 as a potent tumor suppressor in lung cancer growth and metastasis.
...
PMID:ING5 inhibits cancer aggressiveness via preventing EMT and is a potential prognostic biomarker for lung cancer. 2593 45
Multivariable analyses of global expression profiling are valid indicators of the prognosis of various diseases including brain cancers. To identify the candidates for markers of prognosis of glioblastoma, we performed multivariable analyses on the status of epithelial (EPI)-mesenchymal (MES) transition (
EMT
), glioma (GLI) stem cells (GSCs), molecular target therapy (MTT), and potential glioma biomarkers (PGBs) using the expression data and clinical information from patients. Random forest survival and Cox proportional hazards regression analyses indicated significant variable values for
DSG3
,
CLDN1
,
CDH11
,
FN1
,
HDAC3/7
,
PTEN
,
L1CAM
,
OLIG2
,
TIMP4
,
IGFBP2
, and
GFAP
. The analyses also comprised prognosis prediction formulae that could distinguish between the survival curves of the glioblastoma patients. In addition to the genes mentioned above,
HDAC1
,
FLT1
,
EGFR
,
MGMT
,
PGF
,
STAT3
,
SIRT1
, and
GADD45A
constituted complex genetic interaction networks. The calculated status scores obtained by principal component analysis indicated that GLI genes covered the status of EPI, GSC, and MTT-related genes. Moreover, survival tree analyses indicated that MES
high
, MES
high
GLI
low
, GSC
high
GLI
low
, MES
high
MTT
low
, and PGB
high
showed poor prognoses and MES
middle
, GSC
low
, and PGB
low
showed good prognoses, suggesting that enhanced
EMT
and GSC are associated with poor survival and that lower expression of EPI markers and the pre-stages of
EMT
are relatively less malignant in glioblastoma. These results demonstrate that the assessment of
EMT
and GSC enables the prediction of the prognosis of glioblastoma that would help develop novel therapeutics and de novo marker candidates for the prognoses of glioblastoma.
...
PMID:Promising Prognosis Marker Candidates on the Status of Epithelial-Mesenchymal Transition and Glioma Stem Cells in Glioblastoma. 3165 34