Plasmin also activated VEGF-C. As lymphangiogenic growth factors promote the metastatic spread of cancer via the lymphatics, the proteolytic activation of these molecules represents a potential target for antimetastatic agents.
By constructing lentivirus-mediated shVEGF-C cells, VEGF-C down-regulation suppressed LPS' promotive effect on cancer cell motility and HDLEC tube-like formation capacity.
SPARC expression was inversely associated with the degree of malignancy and it had a negative correlation with VEGF-C expression, VEGF-D expression, LVD and MVD which were actually higher for advanced tumors than for non-advanced tumors.
Vascular endothelial growth factor C (VEGF-C), an angiogenic/lymphangiogenic factor with high expression levels in tumor tissues, plays important roles in the development of several malignancies including hepatocellular carcinoma (HCC).
Cancer tissue samples from 92 patients with pN2 non-small-cell lung cancer and benign lung disease tissues samples from 30 patients were examined by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry assays to detect VEGF-C expression.
Northern blot analysis of total RNA revealed an approximately 2.2-fold increase in VEGF-C mRNA transcript in the cancer samples compared with the normal pancreas.
Analysis of VEGF-A and C expression (only in cancer cell lines MCF7, A549 and H460 but not in the ocular cell line RPE19) has shown enhanced expression levels of VEGF-C with increase in knockdown of VEGF-A.
Immunohistochemistry confirmed that P-cadherin expression was cancer specific, and vascular endothelial growth factor-C and MLH1 expression were limited to type I and type II cancers, respectively.