Biosynthesis of copper oxide nanoparticles mediated Annona muricata as cytotoxic and apoptosis inducer factor in breast cancer cell lines

• Published in: Scientific reports Vol. 12; no. 1; p. 16165
• Main Authors: Mahmood, Rana I., Kadhim, Afraa Ali, Ibraheem, Sumayah, Albukhaty, Salim, Mohammed-Salih, Harraa S., Abbas, Ruaa H., Jabir, Majid S., Mohammed, Mustafa K. A., Nayef, Uday M., AlMalki, Faizah A., Sulaiman, Ghassan M., Al-Karagoly, Hassan
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 28-09-2022; Nature Publishing Group; Nature Portfolio
• Subjects: 631/337; 631/67; 639/925; Annona muricata; Apoptosis; Biosynthesis; Breast cancer; Cell death; Cell membranes; Cell proliferation; Copper; Cytotoxicity; Dehydrogenase; Dehydrogenases; Epithelial cells; Humanities and Social Sciences; L-Lactate dehydrogenase; Lactic acid; multidisciplinary; Nanoparticles; Plant extracts; Scanning electron microscopy; Science; Science (multidisciplinary); Spectroscopy; Tumor cell lines
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-20360-y

This study investigated for the first time a simple bio-synthesis approach for the synthesis of copper oxide nanoparticles (CuO NPs) using
Annona muricata L
(
A. muricata
) plant extract to test their anti-cancer effects. The presence of CuONPs was confirmed by UV–visible spectroscopy, Scanning electron microscope (SEM), and Transmission electron microscope (TEM). The antiproliferative properties of the synthesized nanoparticles were evaluated against (AMJ-13), (MCF-7) breast cancer cell lines, and the human breast epithelial cell line (HBL-100) as healthy cells. This study indicates that CuONPs reduced cell proliferation for AMJ-13 and MCF-7. HBL-100 cells were not significantly inhibited for several concentration levels or test periods. The outcomes suggest that the prepared copper oxide nanoparticles acted against the growth of specific cell lines observed in breast cancer. It was observed that cancer cells had minor colony creation after 24 h sustained CuONPs exposure using (IC
50
) concentration for AMJ-13 was (17.04 µg mL
−1
). While for MCF-7 cells was (18.92 µg mL
−1
). It indicates the uptake of CuONPs by cancer cells, triggering apoptosis. Moreover, treatment with CuONPs enhanced Lactate dehydrogenase (LDH) production, probably caused by cell membrane damage, creating leaks comprising cellular substances like lactate dehydrogenase. Hence, research results suggested that the synthesized CuONPs precipitated anti-proliferative effects by triggering cell death through apoptosis.