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In the present work, manganese–copper co-infused nickel oxide nanoparticles (MnCu co-doped NiO NPs) were formulated via a green process using Carica papaya extract. The MnCu co-doped NiO NPs were characterized by X-ray diffraction (XRD), UV–Vis, Fourier transform infrared, field emission scanning electron microscope, energy dispersive X-ray analysis, and photoluminescence (PL) spectrum. The XRD pattern demonstrated that synthesized MnCu co-doped NiO NPs exhibit cubic structure. On the PL spectrum, various surface defects were identified. MnCu co-doped NiO NPs exhibited ferromagnetic properties at 37°C. The antimicrobial activity of green synthesis MnCu co-doped NiO NPs against human pathogens (Escherichia coli, Streptococcus pneumoniae, Bacillus megaterium, Bacillus subtilis, Shigella dysenteriae, Pseudomonas aeruginosa) and Candida albicans as fungal strains were demonstrated. The MnCu co-doped NiO NPs treatment considerably reduced MDA-MB-231 cell viability while not disturbing HBL-100 cell viability. Different fluorescent staining analyses revealed that MnCu co-doped NiO NPs induced nuclear and mitochondrial damage to improve free radical production, altering mitochondrial membrane protein potential, which led to apoptotic cell death in MDA-MB-231 cells. The MnCu co-doped NiO NP treatment enhanced pro-apoptotic protein expression and inhibited the cell cycle at the S phase in MDA-MB-231 cells. This makes it easy, cheap, and environmentally friendly to make MnCu co-doped NiO NPs using C. papaya extract, which has excellent antimicrobial properties.

In this study, we evaluated the antiproliferative and apoptotic properties of Pluronic-F127-containing manganese oxide nanoparticles (PF-127-coated Mn2O3 NPs) derived from the leaf extract of Glycyrrhiza uralensis (GU) on breast adenocarcinoma, MCF7, and MDA-MB-231 cell lines. The leaf extract of GU contains bioactive molecules that act as a reducing or capping agent to form Mn2O3 NPs. Various analytical techniques were used to characterize the physiochemical properties of PF-127-coated Mn2O3 NPs, including spectroscopy (ultralight-Vis, Fourier transform infrared, photoluminescence), electron microscopy (field emission scanning electron microscopy and transmission electron microscopy), X-ray diffraction (XRD), electron diffracted X-ray spectroscopy (EDAX), and dynamic light scattering. The average crystallite size of Mn2O3 NPs was estimated to be 80 nm, and the NPs had a cubic crystalline structure. PF127-encapsulated Mn2O3 NPs significantly reduce MDA-MB-231 and MCF-7 cell proliferation, while increasing endogenous ROS and lowering mitochondrial matrix protein levels. DAPI, EtBr/AO dual staining, and Annexin-V-FITC-based flow cytometry analysis revealed that PF127-coated Mn2O3 NP-treated breast cancer cells exhibit nuclear damage and apoptotic cell death, resulting in cell cycle arrest in the S phase. Furthermore, PF127-encapsulated Mn2O3 NPs show strong antimicrobial efficacy against various strains. As a result, we can conclude that PF127-coated Mn2O3 NPs may be effective as future anticancer agents and treatment options for breast cancer.

The present study investigated the cytotoxicity and proapoptotic properties of iron oxide-sodium-alginate-thymoquinone nanocomposites against breast cancer MDA-MB-231 cells in vitro and in silico. This study used chemical synthesis to formulate the nanocomposite. Electron microscopies such as scanning (SEM) and transmission (TEM), Fourier transform infrared (FT-IR), Ultraviolet-Visible, Photoluminescence spectroscopy, selected area (electron) diffraction (SAED), energy dispersive X-ray analysis (EDX), and X-ray diffraction studies (XRD) were used to characterize the synthesized ISAT-NCs and the average size of them was found to be 55 nm. To evaluate the cytotoxic, antiproliferative, and apoptotic potentials of ISAT-NCs on MDA-MB-231 cells, MTT assays, FACS-based cell cycle studies, annexin- V -PI staining, ELISA, and qRT-PCR were used. PI3K-Akt-mTOR receptors and thymoquinone were predicted using in-silico docking studies. Cell proliferation is reduced in MDA-MB-231 cells due to ISAT-NC cytotoxicity. As a result of FACS analysis, ISAT-NCs had nuclear damage, ROS production, and elevated annexin- V levels, which resulted in cell cycle arrest in the S phase. The ISAT-NCs in MDA-MB-231 cells were found to downregulate PI3K-Akt-mTOR regulatory pathways in the presence of inhibitors of PI3K-Akt-mTOR, showing that these regulatory pathways are involved in apoptotic cell death. We also predicted the molecular interaction between thymoquinone and PI3K-Akt-mTOR receptor proteins using in-silico docking studies which also support PI3K-Akt-mTOR signaling inhibition by ISAT-NCs in MDA-MB-231 cells. As a result of this study, we can conclude that ISAT-NCs inhibit the PI3K-Akt-mTOR pathway in breast cancer cell lines, causing apoptotic cell death. [Display omitted] [ABSTRACT FROM AUTHOR]