Aberrant factors associated with fibrinolysis and thrombosis are found in many cancer patients, which can promote metastasis and are associated with poor prognosis. The relationship between tumor-associated fibrinolysis and thrombosis is poorly understood in pancreatic cancer. This review provides a brief highlight of existing studies that the fibrinolysis and coagulation systems were activated in pancreatic cancer patients, along with aberrant high concentrations of tissue plasminogen activator (t-PA), urine plasminogen activator (u-PA), D-dimer, fibrinogen, or platelets. These factors cooperate with each other, propelling tumor cell shedding, localization, adhesion to distant metastasis. The relationship between thrombosis or fibrinolysis and cancer immune escape is also investigated. In addition, the potential prevention and therapy strategies of pancreatic cancer targeting factors in fibrinolysis and coagulation systems are also been discussed, in which we highlight two effective agents aspirin and low-molecular weight heparin (LMWH). Summarily, this review provides new directions for the research and treatment of pancreatic cancer.

Studies have revealed that β‑asarone exerts a powerful inhibitory effect on the proliferation of human cancer cells. The authors' previous study demonstrated that β‑asarone could induce LoVo colon cancer cell apoptosis in vitro and in vivo, indicating its anticancer properties. The present study aimed to determine the antineoplastic effect of β‑asarone in HCT116 colon cancer cells. An in vitro proliferation assay using a real time cell analyzer demonstrated that β‑asarone effectively decreased HCT116 cell proliferation in a dose‑dependent manner. Bioinformatics analysis revealed that differentially expressed genes following β‑asarone inhibition were involved in the ‘cell cycle’, ‘cell division’, ‘cell proliferation’ and ‘apoptosis’. Subsequently, a xenograft assay evidenced the inhibitory effect of β‑asarone on the growth of HCT116 tumors in vivo. Further detection of immune‑associated cytokines and cells suggested that β‑asarone might be involved in the antitumor immune response by stimulating granulocyte‑colony stimulating factor and increasing the number of macrophage cells in the spleen. Additionally, a murine model of splenic‑transplantation verified the strong suppressive role of β‑asarone in colon cancer liver metastasis in vivo. Taken together, the results of the current study revealed that β‑asarone decreased HCT116 colon cancer cell proliferation and liver metastasis potentially by activating the innate immune system, supporting the multi‑system regulation theory and providing a basis for further mechanistic studies on colon cancer.