Volume 34, Issue 4 (12-2025)
JGUMS 2025, 34(4): 438-453 |
Back to browse issues page
Research code: 0
Ethics code: IR.YAZD.REC.1402.058
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Zamani F, Nematzadeh Soteh N, Heidari M M, Chamani R, Khatami M, Moradi A. The Effect of Tumstatin and Canstatin-Derived Angiogenesis Inhibitor Peptides on FAK Expression in an Animal Model of Breast Cancer. JGUMS 2025; 34 (4) :438-453
URL: http://journal.gums.ac.ir/article-1-2776-en.html
URL: http://journal.gums.ac.ir/article-1-2776-en.html
Fatemeh Zamani1 
, Niloofar Nematzadeh Soteh1 , Mohammad Mehdi Heidari1 , Reyhane Chamani *1 , Mehri Khatami1 , Ali Moradi2
, Niloofar Nematzadeh Soteh1 , Mohammad Mehdi Heidari1 , Reyhane Chamani *1 , Mehri Khatami1 , Ali Moradi2
1- Department of Biology, Faculty of Science, Yazd University, Yazd, Iran.
2- Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
2- Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Abstract: (751 Views)
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.
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.
Review Paper: Research |
Subject:
Special
Received: 2025/03/1 | Accepted: 2025/05/5 | Published: 2026/01/1
Received: 2025/03/1 | Accepted: 2025/05/5 | Published: 2026/01/1
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
Copyright © The Author(s);
This is an open access article distributed under the terms of the
Creative Commons Attribution License (CC-By-NC),which permits use, distribution, and reproduction in any medium,
provided the original work is properly cited and is not used forcommercial purposes.
Contact Information
