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)
Reduced connexin expression and loss of gap junction function is a characteristic of many cancers, including lung cancer. However, there are little reports about the relation between
Cx31.1
and lung cancer. This study was conducted to investigate the effect of
Cx31.1
on non-small cell lung cancer (NSCLC). We found that the
Cx31.1
was down-regulated in NSCLC cell lines, and the expression levels were reversely related with their metastatic potential. We ectopically expressed
Cx31.1
in H1299 NSCLC cell line to examine the influence of
Cx31.1
overexpression. The results showed that overexpression of
Cx31.1
in H1299 cells reduced cell proliferation, induced a delay in the G(1) phase, inhibited anchorage-independent growth and suppressed cell migration and invasion. The cell cycle delay and cell migration and invasion suppressive effects of
Cx31.1
were partially reversed by siRNA targeting mRNA of
Cx31.1
. Moreover, xenografts of
Cx31.1
overexpressing H1299 cells showed reduced tumourigenicity. These results suggested that
Cx31.1
has tumour-suppressive properties. Further investigation indicated that cyclin D3 may be responsible for
Cx31.1
-induced G(1) phase delay. Importantly,
Cx31.1
increased the expression of epithelial markers, such as cytokeratin 18, and decreased expression of mesenchymal markers, such as vimentin, indicating a
Cx31.1
-mediated partial shift from a mesenchymal towards an epithelial phenotype. We concluded that
Cx31.1
inhibit the malignant properties of NSCLC cell lines, the mechanisms under this may include regulation of
EMT
.
...
PMID:Cx31.1 acts as a tumour suppressor in non-small cell lung cancer (NSCLC) cell lines through inhibition of cell proliferation and metastasis. 2177 77
