IL-6 promotes tumor growth by VEGF-dependent angiogenesis via a STAT3 pathway.(interleukin-6; vascular endothelial growth factor)

2003 MAY 1 - (NewsRx.com & NewsRx.net) -- Interleukin-6 may promote cervical tumorigenesis by vascular endothelial growth factor-dependent angiogenesis via a STAT3 pathway, study results suggest.

Interleukin-6 (IL-6) is suspected to be involved in cervical cancer pathogenesis. Researchers in Taiwan set out to identify specifically how.

They reported finding that "IL-6 promotes in vivo tumor growth of human cervical cancer C33A cells, but does not substantially alter their in vitro growth kinetics.

"The in vivo angiogenic assays showed that IL-6 increases angiogenic activity in human cervical cancer cells, an effect that is specifically associated with upregulation of vascular endothelial growth factor (VEGF). Also, using anti-VEGF antibody to block VEGF function significantly inhibited IL-6-mediated angiogenesis and tumor growth in nude mice, strongly supporting the critical role of VEGF in the IL-6-mediated cervical tumorigenesis," wrote L.H. Wei and colleagues.

This finding prompted the researchers to take a look at the "signaling pathway downstream of IL-6/IL-6R responsible for the regulation of VEGF."

"Notably," they said, "pharmacological inhibition of PI3-K or MAPK failed to inhibit IL-6-mediated transcriptional upregulation of VEGF. Meanwhile, blocking [the] STAT3 pathway with dominant-negative mutant STAT3D effectively abolished IL-6-induced VEGF mRNA. In transient transfections, a luciferase reporter ...