Pancreatic cancers are classified based on where they occur, and are grouped into those derived from exocrine and those derived from
neuroendocrine tumors, thereby experiencing different anticancer effects under medication. Therefore, it is necessary to develop anticancer drugs that can inhibit both types. To this end, we developed a
heparin-
taurocholate conjugate, i.e., LHT, to suppress
tumor growth via its antiangiogenic activity. Here, we conducted a study to determine the anticancer efficacy of LHT on pancreatic ductal
adenocarcinoma (PDAC) and pancreatic
neuroendocrine tumor (
PNET), in an orthotopic animal model. LHT reduced not only proliferation of
cancer cells, but also attenuated the production of
VEGF through ERK dephosphorylation. LHT effectively reduced the migration, invasion and tube formation of endothelial cells via dephosphorylation of VEGFR, ERK1/2, and FAK
protein. Especially, these effects of LHT were much stronger on
PNET (RINm cells) than PDAC (PANC1 and MIA PaCa-2 cells). Eventually, LHT reduced ~50% of the
tumor weights and
tumor volumes of all three
cancer cells in the orthotopic model, via antiproliferation of
cancer cells and antiangiogenesis of endothelial cells. Interestingly, LHT had a more dominant effect in the
PNET-induced
tumor model than in PDAC in vivo. Collectively, these findings demonstrated that LHT could be a potential antipancreatic
cancer medication, regardless of
pancreatic cancer types.