Background Canstatin and tumstatin are proteins derived from collagen IV that inhibit tumor growth by preventing angiogenesis. Increased focal adhesion kinase (FAK) expression may promote tumor progression and metastasis by stimulating the proliferation of cancer cell and angiogenesis. 
Objective This study aimed to investigate the effects of peptides derived from Canstatin and Tumstatin on breast tumor growth in an animal model and on the expression of FAK in tumor tissue. 
Methods Tumors were induced in mice by injecting 4T1 cell lines into their flank. The treatment groups were injected intraperitoneally with 5 mg/kg/day of the peptides for 12 days, while the control group received an equal volume of buffer. Tumor sizes were measured, and tumor volume was calculated using the formula v=(the smallest diameter)2×(the largest diameter)×0.52. Ultimately, the tumors were removed, and ribonucleic acid (RNA) was extracted from the tissues. Complementary DNA (cDNA) synthesis was performed using primers designed for the GAPDH gene as a reference gene, FAK, and the polymerase chain reaction (PCR) method was employed. Gene expression was measured using reverse transcription-PCR (RT-PCR) and ΔCT calculation for treatment and control samples. 
Results The peptides derived from Canstatin and Tumstatin inhibited tumor growth by 51% and 49%, respectively, compared to the control group (P<0.05). Additionally, these peptides reduced FAK expression by 69% and 67%, respectively, compared to the control (P<0.05). 
Conclusion The present study confirmed the antitumor effects of these peptides and demonstrated that FAK expression reduction in tumors may be one of their antiangiogenic and anticancer mechanisms. The present results may aid in the design of new anticancer peptide drugs.