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We also found that resveratrol induced the expression of the SOCS-1 protein and mRNA.
Conclusion: Our results suggest that resveratrol blocks STAT3 signaling pathway through induction of SOCS-1, thus attenuating STAT3 phosphorylation and proliferation in SCCHN cells.
Specifically, the SH2 domain of SOCS-1 directly binds to the activation loop of JAKs (Yasukawa et al.
The following pairs of forward and reverse primer sets were used SOCS-1 (5'ACGCAGGATTAACGTGGATG-3' and 5'-CCCTGGTTTGTGCAAAGATACT3'), Cyclin D1, (5'-ACAAGCTCTGCATCTACACCGACA-3' and 5'-AGAAGCTGTGCATCTACACCGACA-3').
FaDu cells were transfected with 50 nM of SOCS-1 siRNA or scrambled siRNA using serum-free Lipofectamine2000 (Invitrogen) according to the manufacturer's protocols and treated 24 h post-transfection.
Resveratrol induced the expression of SOCS-1 and SOCS-1 mRNA
We examined whether resveratrol can modulate the expression of SOCS-1 in FaDu cells.
Deletion of SOCS-1 expression by siRNA reversed the inhibition of STAT3activation by resveratrol
We determined whether the suppression of SOCS-1 expression by siRNA would abrogate the inhibitory effect of resveratrol on STAT3 activation.
Interestingly, resveratrol triggered the expression of SOCS-1 protein, which is known as a negative regulator of STAT3 activation.
SOCS-1 has been shown to be involved in the negative regulation of IL-6R/JAK-mediated activation of STAT3 and the expression of SOCS-1 following demethylation or transient transfection can suppresses STAT3 activation in HNSCC cells (Lee et al.
Overall, our results indicate for the first time that resveratrol can inhibit constitutive STAT3 signaling pathway through upregulation of SOCS-1 protein in HNSCC cells, as well as can enhance the effects of radiotherapy through the downregulation of gene products that mediate tumor cell survival, proliferation, invasion, and metastasis in HNSCC.
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