Knockdown of Sema4D in WSU-HN6 cells inhibited collagen production by fibroblasts, and decreased activated TGF-β1 levels in culture medium of HNSCC cell lines.
Our results suggest that HNSCC patients who exhibit persistently elevated sMICA and TGF-β1 levels after CRT are at higher risk of tumor progression or death.
It was thus the aim of this study to test the hypothesis that TGF-β1 modulates the interactions of tumor transition between BMSCs and HNSCC, affecting the expression of E-cadherin, Vimentin, Snail, Twist, MMP14 and beta-catenin.
Thus, our findings suggest that cytoplasmic DRAK1 increases tumorigenic potential through inhibition of TGF-β1-mediated tumor suppressor activity in HNSCC cells and may be a potential therapeutic target for HNSCCs.
We have recently shown that the single nucleotide polymorphism (SNP) rs1982073 of the TGFbeta1 gene (TGFB1) is associated with the survival of HNSCC patients who have undergone CRT.
In addition to the above changes in tumor epithelia, both normal head and neck tissue and HNSCC from HN-Smad4-/- mice exhibited severe inflammation, which was associated with increased expression of TGF-beta1 and activated Smad3.
In response to recombinant TGFbeta1, both growth inhibition and TGFbeta target gene modulation were attenuated or absent in a panel of human HNSCC lines.
Tissue specimens of HNSCC (n = 22) and normal oral mucosa (n = 8) were analysed by real-time, quantitative PCR assays for CCN2 and TGF-beta1 expression.