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:C1522282 (
EMT
)
2,868
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Neuroblastoma (NB) is the most common malignant tumor in infancy and most common extracranial solid tumor in childhood. With the improvement of diagnosis and treatment, the survival rate of patients with low-risk and intermediate-risk NB can reach up to 90%. In contrast, for high-risk NBs, the long-term survival rate is still <40% because of heterogeneity of this tumor. The pathogenesis of NB is still not explicit, therefore it is of great significance to explore the mechanism of NB tumorigenesis and discover new therapeutic targets for NB.
Polo-like kinase 4
(
PLK4
), one of the polo-like kinase family members, is an important regulator of centriole replication. The aberrant expression of
PLK4
was found in several cancers and a recent study has unraveled a novel function of
PLK4
as a mediator of invasion and metastasis in Hela and U2OS cells. However, the function of
PLK4
in NB development and progression remains to be elucidated. The study showed the expression level of
PLK4
in NB tissues was remarkably upregulated and high expression of
PLK4
was negatively correlated with clinical features and survival, which suggested that
PLK4
could be a potential tumor-promoting factor of NB. Functional studies indicated downregulation of
PLK4
suppressed migration and invasion and promoted apoptosis in NB cells. Further experiments showed that downregulation of
PLK4
in NB cells inhibited
EMT
through the PI3K/Akt signaling pathway. Animal experiments demonstrated that the downregulation of
PLK4
in SK-N-BE(2) cells dramatically suppressed tumorigenesis and metastasis.
PLK4
may be a promising therapeutic target for NB.
...
PMID:Polo-like kinase 4 mediates epithelial-mesenchymal transition in neuroblastoma via PI3K/Akt signaling pathway. 2935 13
