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Resibufogenin ( RB ), one of the major active compounds of the traditional Chinese medicine Chansu, has received considerable attention for its potency in cancer therapy. However, the anticancer effects and the underlying mechanisms of  RB  on pancreatic cancer remain elusive. Here, we found that  RB  inhibited the viability and induces caspase‐dependent apoptosis in human pancreatic cancer cells Panc‐1 and Aspc. Resibufogenin‐induced apoptosis was through inhibition of constitutive nuclear factor‐κB ( NF ‐κB) activity and its target genes’ expression, which was caused by downregulation of transforming growth factor‐β‐activated kinase 1 ( TAK 1) levels and suppression of IκB kinase activity in Panc‐1 and Aspc cells. This induction of  TAK 1‐mediated  NF ‐κB inactivation by  RB  was associated with increased glycogen synthase kinase‐3 ( GSK ‐3) phosphorylation and subsequent suppression of its activity. Moreover,  RB ‐induced  GSK ‐3 phosphorylation/inactivation acted through activation of protein kinase C but not Akt. Finally,  RB  suppressed human pancreatic tumor xenograft growth in athymic nude mice. Thus, our findings reveal a novel mechanism by which  RB  suppresses  TAK 1‐mediated  NF ‐κB activity through protein kinase C‐dependent inhibition of  GSK ‐3. Our findings provide a rationale for the potential application of  RB  in pancreatic cancer therapy.

cancer science

Resibufogenin suppresses transforming growth factor‐β‐activated kinase 1‐mediated nuclear factor‐κB activity through protein kinase C‐dependent inhibition of glycogen synthase kinase 3