Tranexamic acid reduces endometrial cancer effects through the production of angiostatin

Area of Science:

• Oncology
• Inflammation Research
• Pharmacology

Background:

• Tranexamic acid (TA) shows potential antitumor effects in preclinical cancer models.
• The precise mechanisms of TA's action against endometrial cancer are not fully understood.
• Chronic inflammation is implicated in endometrial cancer development.

Purpose of the Study:

• To investigate the efficacy of tranexamic acid (TA) in a mouse model of chronic inflammation-associated endometrial cancer.
• To elucidate the underlying molecular mechanisms of TA's antitumor effects in this model.

Main Methods:

• Endometrial cancer was induced in mice using N-methyl-N-nitrosourea (MNU) and estradiol.
• Mice received TA (12 mg/kg) three times weekly post-cancer induction.
• Plasma markers (carbohydrate antigen 125, IL-6, TNF-α), plasminogen/plasmin levels, and macrophage/MMP-12/angiostatin in uterine tumors were analyzed.

Main Results:

• TA administration ameliorated endometrial cancer development and suppressed key inflammatory markers (CA125, IL-6, TNF-α).
• TA treatment modulated plasminogen and plasmin levels, increasing plasminogen while decreasing plasmin.
• Macrophage counts and levels of MMP-12 and angiostatin within uterine tumors were elevated by TA treatment.

Conclusions:

• Tranexamic acid (TA) demonstrates efficacy in ameliorating MNU and estradiol-induced endometrial cancer in mice.
• TA exerts its antitumor effects by regulating the macrophage/MMP-12/plasminogen/angiostatin signaling pathway.
• This study provides mechanistic insights into TA's therapeutic potential for endometrial cancer.