Mon, May 25, 2026
1- Medical Laboratory research Center, Golestan University of Medical Sciences, Gorgan, Iran
2- 2Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
3- 3Health Management and Social Development Research Center, Department of Biostatistics and Epidemiology, Faculty of Health, Golestan University of Medical Sciences, Gorgan, Iran
4- 4Laboratories of Imam Al-Sadiq Hospital, Ministry of Health, Babylon Governorate, Iraq; Medical Laboratory research Center, Golestan University of Medical Sciences, Gorgan, Iran
5- 5Neonatal and Children’s Health Research Center, Golestan University of Medical Sciences, Gorgan, Iran ,rashidbaghan@yahoo.com
2- 2Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
3- 3Health Management and Social Development Research Center, Department of Biostatistics and Epidemiology, Faculty of Health, Golestan University of Medical Sciences, Gorgan, Iran
4- 4Laboratories of Imam Al-Sadiq Hospital, Ministry of Health, Babylon Governorate, Iraq; Medical Laboratory research Center, Golestan University of Medical Sciences, Gorgan, Iran
5- 5Neonatal and Children’s Health Research Center, Golestan University of Medical Sciences, Gorgan, Iran ,
Abstract: (359 Views)
Background: The high global mortality of breast cancer in women necessitates novel therapies with fewer side effects.. Urtica dioica agglutinin (UDA), a lectin from stinging nettle, exhibits antiproliferative properties in various cancers, but its effect on breast cancer cells remain underexplored. This study evaluates UDA’s cytotoxic potential against Michigan Cancer Foundation-7 (MCF-7) breast cancer cells while assessing its impact on non-tumorigenic human mammary epithelial (MCF-10A) and Human embryonic kidney (HEK-293) cells.
Methods: UDA purification was performed via affinity chromatography from Urtica dioica rhizomes, confirmed by SDS-PAGE (8.5–9.5 kDa) and agglutination assays. MCF-7, MCF-10A, and HEK-293 cells were treated with different concentrations of UDA (7.5–480 µg/ml) for 24 and 48 hours. Cytotoxicity was assessed using MTT assays to measure cell viability.
Results: UDA significantly inhibited MCF-7 proliferation in a dose- and time-dependent manner (P < 0.01 at 24 hours; P < 0.0001 at 48 hours). At 240 µg/ml (during 48 hours), viability dropped below 50%, while normal HEK-293 cells showed <30% toxicity. MCF-10A proliferation remained unaffected, even at 480 µg/ml. IC50 was 389.7 207.0 μg/mL for 24 and 48 hours.
Conclusion: UDA targets breast cancer cells (MCF-7) with minimal toxicity to normal cells, positioning it as a promising anticancer candidate. Determining the mechanism of its action and apoptosis-inducing potential needs further research in the future. .
Methods: UDA purification was performed via affinity chromatography from Urtica dioica rhizomes, confirmed by SDS-PAGE (8.5–9.5 kDa) and agglutination assays. MCF-7, MCF-10A, and HEK-293 cells were treated with different concentrations of UDA (7.5–480 µg/ml) for 24 and 48 hours. Cytotoxicity was assessed using MTT assays to measure cell viability.
Results: UDA significantly inhibited MCF-7 proliferation in a dose- and time-dependent manner (P < 0.01 at 24 hours; P < 0.0001 at 48 hours). At 240 µg/ml (during 48 hours), viability dropped below 50%, while normal HEK-293 cells showed <30% toxicity. MCF-10A proliferation remained unaffected, even at 480 µg/ml. IC50 was 389.7 207.0 μg/mL for 24 and 48 hours.
Conclusion: UDA targets breast cancer cells (MCF-7) with minimal toxicity to normal cells, positioning it as a promising anticancer candidate. Determining the mechanism of its action and apoptosis-inducing potential needs further research in the future. .
Research Article: Research Article |
Subject:
Molecular Medicine
Received: 2025/06/2 | Accepted: 2026/02/8
Received: 2025/06/2 | Accepted: 2026/02/8
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