Proinflammatory Cytokines IL-6 and TNF-α Increased Telomerase Activity through NF-κB/STAT1/STAT3 Activation, and Withaferin A Inhibited the Signaling in Colorectal Cancer Cells

<div>STAT3 dimerize with STAT1 and STAT1 dimerize with NF-κB. Withaferin A abolished the protein-protein interactions. (a) STAT1 was heterodimerized with STAT3 from the pull-down assay with an STAT3 antibody. The binding affinity was increased upon IL-6 and TNF-α cotreatments. (b) Withaferin A (10 μM) treatment has abolished the STAT3-STAT1 interactions. (c) Coimmunoprecipitation with STAT1 antibody revealed that STAT1 was bound to NF-κB. STAT1-NF-κB interaction was enhanced by the IL-6 and TNF-α stimulation. (d) These interactions were also abolished by withaferin A (10 μM) treatment.</div>

Mediators of Inflammation

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Figure 6

Figure 6: Proinflammatory Cytokines IL-6 and TNF-α Increased Telomerase Activity through NF-κB/STAT1/STAT3 Activation, and Withaferin A Inhibited the Signaling in Colorectal Cancer Cells

Figure 6 | Proinflammatory Cytokines IL-6 and TNF-α Increased Telomerase Activity through NF-κB/STAT1/STAT3 Activation, and Withaferin A Inhibited the Signaling in Colorectal Cancer Cells 