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Pancreatic cancer is the leading cause of cancer death worldwide with a poor survival rate. The objective of this study was to determine the mechanism of action of a novel antimitotic and Stat3 inhibitor, LTP-1, on human pancreatic cancer  in vitro  and  in vivo . We found that LTP-1 inhibited pancreatic cancer cell growth and viability with significant G 2 /M arrest and disruption of microtubule dynamics. LTP-1 also caused G 2 /M arrest-independent Stat3 dephosphorylation along with ERK activation, which indicated the possible dual function of LTP-1. Long-term treatment of LTP-1 also induced polyploidy, activated caspases, induced subG 1  cell population, and therefore, triggered pancreatic cancer cell apoptosis. Finally, we used an  in viv o xenograft model to demonstrate that LTP-1 suppressed the growth of pancreatic adenocarcinoma. In summary, our data suggest that LTP-1 may alter microtubule dynamics, which ultimately causes polyploidy and apoptosis, thereby inhibiting pancreatic cancer growth  in vitro  and  in vivo . This study provides evidence that LTP-1 could be a potential therapeutic agent for further development of pancreatic cancer treatment.

LTP-1, a novel antimitotic agent and Stat3 inhibitor, inhibits human pancreatic carcinomas in vitro and in vivo