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:C0019204 (
hepatocellular carcinoma
)
71,386
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Activation of YAP/TEAD signaling is very common in the progression of
HCC
(
Hepatocellular carcinoma
). Nuclear pore complex (NPC) regulates the shuttling of proteins between cytoplasm and nucleus. Nuclear accumulation of YAP protein has been observed in the majority of
HCC
tissues. However, whether NPC could regulate the YAP/TEAD signaling remains unknown. In this study, it was found
NUP37
, the component of NPC, significantly up-regulated in
HCC
clinical samples and mouse model. Over-expression of
NUP37
promoted the growth, migration and invasion of
HCC
cells, while knocking down the expression of
NUP37
inhibited the growth, migration, invasion and metastasis of
HCC
cells and improved the survival of the mouse model.
NUP37
interacted with YAP and activated YAP/TEAD signaling by enhancing the interaction between YAP and TEAD. Taken together, these data demonstrated the oncogenic roles of
NUP37
in the progression of
HCC
and suggested that
NUP37
might be a promising therapeutic target.
...
PMID:NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma. 2922 69
NUP37
has been reported as a component of the nuclear pore complex, which may be involved in tumorigenesis. Previous reports have shown that
NUP37
acts as an oncogene in the development of
hepatocellular carcinoma
. However, its role in lung cancer remains unknown. The present study demonstrated for the first time that
NUP37
expression was overexpressed in non-small cell lung cancer (NSCLC) samples compared with the corresponding expression noted in normal tissues. The results were derived by analyzing public datasets. Moreover, it was shown that
NUP37
was overexpressed in advanced stage NSCLC samples compared with the corresponding expression of this protein in early stage NSCLC samples. Higher expression levels of
NUP37
correlated with lower overall survival (OS) in NSCLC samples. Bioinformatic analysis indicated that
NUP37
was involved in regulating cell cycle progression in NSCLC. Furthermore, knockdown of
NUP37
suppressed cell growth and proliferation in A549and H1299 cells as demonstrated with the Celigo Cell Counting method and the MTT assay. Flow cytometry analysis indicated that knockdown of
NUP37
induced significant S phage cell arrest and apoptosis in A549 and H1299 cells. The results showed that knockdown of
NUP37
remarkably induced the protein levels of cleaved PARP, P53 and BCL2 in A549 cells. Therefore, it was concluded that
NUP37
serves a distinguished role in the growth of lung cancer cells and may be considered as a potential biomarker and therapeutic target for lung cancer.
...
PMID:NUP37 silencing induces inhibition of cell proliferation, G1 phase cell cycle arrest and apoptosis in non-small cell lung cancer cells. 3201 8
