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Target Concepts:
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Query: UMLS:C0546837 (
esophageal cancer
)
8,907
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Vascular endothelial growth factor C
(
VEGF-C
) is known to act in lymphangiogenesis. Recent reports suggest
VEGF-C
plays a role in the spread of several cancers to the lymph system. Lymphatic spread is a critical prognostic factor in
esophageal cancer
, however, the molecular mechanism involved in the spread of cancerous cells remains unclear. In the present study the clinicopathological implication of
VEGF-C
was analyzed using immunohistochemistry. Seventy-one patients with esophageal squamous cell carcinoma (ESCC) resected in our institute were included in this study. Formalin-fixed paraffin-embedded specimens were stained for
VEGF-C
and the correlation between the staining, its clinicopathological parameters and its prognostic power were analyzed statistically. Only histological grade (differentiation) was shown to have a statistically significant correlation with
VEGF-C
expression (p=0.028). Age (p=0.064), lymph node metastasis (pN) (p=0.085) and vascular invasion (p=0.092) tended to correlate with
VEGF-C
expression although on analysis this correlation was not statistically significant. The results suggested there is no prognostic implication for
VEGF-C
in ESCC (p=0.80). There is no significant correlation between
VEGF-C
expression and clinicopathological parameters involved in lymphatic spread. However,
VEGF-C
expression might play an important role in metastasis of ESCC since histological grade was closely related to lymph node metastasis and distant metastasis.
...
PMID:VEGF-C expression correlates with histological differentiation and metastasis in squamous cell carcinoma of the esophagus. 1216 62
Vascular endothelial growth factor C
(
VEGF-C
) is a key regulator of angiogenesis and lymphangiogenesis.
VEGF-C
is also implicated in the development of
esophageal cancer
. We investigated the mRNA levels of
VEGF-C
and its receptors in 38 esophageal squamous cell carcinoma specimens (ESCCs) and matched adjacent normal esophageal tissues via real-time PCR. The mRNA levels of
VEGF-C
, VEGFR-2 and VEGFR-3 were significantly upregulated in ESCCs versus respective side normal tissues. To explore the influence of
VEGF-C
on
esophageal cancer
progression, the expression of
VEGF-C
was manipulated in
esophageal cancer
cell lines TE-1 and Eca-109.
VEGF-C
transcription, translation and secretion were significantly enhanced in cells stably transfected with a
VEGF-C
overexpression vector or attenuated in
VEGF-C
shRNA-transfected cell lines. In vitro, TE-1 cells stably transfected with a
VEGF-C
overexpression vector exhibited an increased rate of cell proliferation, migration and focus formation, whereas knockdown of
VEGF-C
inhibited cell proliferation, migration and focus formation. Similar results were obtained for Eca-109 cells.
VEGF-C
mediated biological function through transcription of CNTN-1, which is implicated in tumor invasion and metastasis. The expression of
VEGF-C
was correlated with that of CNTN-1 and cell proliferation and migration induced by
VEGF-C
were reversed by silencing of CNTN-1. In addition, nude mice inoculated with
VEGF-C
shRNA-transfected cells exhibited a significantly decreased tumor size in vivo via reduced VEGFR-2 and VEGFR-3 phosphorylation and microvessel formation.
VEGF-C
upregulation may be involved in esophageal tumor progression. Vector-based RNA interference (RNAi) targeting
VEGF-C
is a potential therapeutic method for human esophageal carcinoma.
...
PMID:VEGF-C promotes the development of esophageal cancer via regulating CNTN-1 expression. 2148 72
