Marine Natural Compound (Neviotin A) Displays Anticancer Efficacy by Triggering Transcriptomic Alterations and Cell Death in MCF-7 Cells.

We investigated the anticancer mechanism of a chloroform extract of marine sponge (Haliclona fascigera) (sample C) in human breast adenocarcinoma (MCF-7) cells. Viability analysis using MTT and neutral red uptake (NRU) assays showed that sample C exposure decreased the proliferation of cells. Flow cytometric data exhibited reactive oxygen species (ROS), nitric oxide (NO), dysfunction of mitochondrial potential, and apoptosis in sample C-treated MCF-7 cells. A qPCR array of sample C-treated MCF-7 cells showed crosstalk between different pathways of apoptosis, especially BIRC5, BCL2L2, and TNFRSF1A genes. Immunofluorescence analysis affirmed the localization of p53, bax, bcl2, MAPKPK2, PARP-1, and caspase-3 proteins in exposed cells. Bioassay-guided fractionation of sample C revealed Neviotin A as the most active compound triggering maximum cell death in MCF-7, indicating its pharmacological potency for the development of a drug for the treatment of human breast cancer.

Iron oxide nanoparticles induced cytotoxicity, oxidative stress, cell cycle arrest, and DNA damage in human umbilical vein endothelial cells.

BACKGROUND: Nanotechnology and material science have developed enormously fast in recent years. Due to their excellent magnetic properties, iron oxide nanoparticles (IONPs) have been broadly applied in the field of bioengineering and biomedical. Thus, it is important to evaluate the safety issues and health effects of these nanomaterials. The present investigation was aimed to evaluate the adverse effects of IONPs on human umbilical vein endothelial cells (HUVECs). METHODS: The cytotoxic potential of IONPs was assessed by MTT and neutral red uptake (NRU) assays. The impact of IONPs on oxidative stress markers (glutathione (GSH) and lipid peroxidation (LPO)), reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) was also examined. Furthermore, the toxic effect of IONPs was quantified by assessing DNA damage, cell cycle arrest, and apoptosis by quantitative real time PCR. RESULTS: We found that IONPs induce a dose-dependent cytotoxicity on HUVECs with IC50 value of 79.13 µg/mL. The results also displayed that IONPs induce oxidative stress, ROS production, and mitochondrial membrane dysfunction. The comet assay results exhibited IONPs induces DNA damage in HUVECs. We found significant cell cycle arrest at SubG1 phase in treated cells and consequent cell death was evidenced by microscopic analysis. Moreover, IONPs display substantial up-regulation of pro-apoptotic genes and down-regulation of anti-apoptotic gene evidenced by real time qPCR. CONCLUSION: Overall, our results clearly demonstrated that IONPs have the potential to induce cytotoxicity, DNA damage, cell cycle arrest, and apoptosis in HUVECs mediated through oxidative stress and ROS production. Thus, IONPs are cytotoxic and it should be handled with proper care.

Effectiveness of Nonfunctionalized Graphene Oxide Nanolayers as Nanomedicine against Colon, Cervical, and Breast Cancer Cells.

Recent studies in nanomedicine have intensively explored the prospective applications of surface-tailored graphene oxide (GO) as anticancer entity. However, the efficacy of nonfunctionalized graphene oxide nanolayers (GRO-NLs) as an anticancer agent is less explored. In this study, we report the synthesis of GRO-NLs and their in vitro anticancer potential in breast (MCF-7), colon (HT-29), and cervical (HeLa) cancer cells. GRO-NLs-treated HT-29, HeLa, and MCF-7 cells showed cytotoxicity in the MTT and NRU assays via defects in mitochondrial functions and lysosomal activity. HT-29, HeLa, and MCF-7 cells treated with GRO-NLs exhibited substantial elevations in ROS, disturbances of the mitochondrial membrane potential, an influx of Ca2+, and apoptosis. The qPCR quantification showed the upregulation of caspase 3, caspase 9, bax, and SOD1 genes in GRO-NLs-treated cells. Western blotting showed the depletion of P21, P53, and CDC25C proteins in the above cancer cell lines after GRO-NLs treatment, indicating its function as a mutagen to induce mutation in the P53 gene, thereby affecting P53 protein and downstream effectors P21 and CDC25C. In addition, there may be a mechanism other than P53 mutation that controls P53 dysfunction. We conclude that nonfunctionalized GRO-NLs exhibit prospective biomedical application as a putative anticancer entity against colon, cervical, and breast cancers.

Development of Metallo (Calcium/Magnesium) Polyurethane Nanocomposites for Anti-Corrosive Applications.

Long-term corrosion protection of metals might be provided by nanocomposite coatings having synergistic qualities. In this perspective, rapeseed oil-based polyurethane (ROPU) and nanocomposites with calcium and magnesium ions were designed. The structure of these nanocomposites was established through Fourier-transform infrared spectroscopy (FT-IR). The morphological studies were carried out using scanning electron microscopy (SEM) as well as transmission electron microscopy (TEM). Their thermal characteristics were studied using thermogravimetric analysis (TGA). Electrochemical experiments were applied for the assessment of the corrosion inhibition performance of these coatings in 3.5 wt. % NaCl solution for 7 days. After completion of the test, the results revealed a very low icorr value of 7.73 × 10-10 A cm-2, a low corrosion rate of 8.342 × 10-5 mpy, impedance 1.0 × 107 Ω cm2, and phase angle (approx 90°). These findings demonstrated that nanocomposite coatings outperformed ordinary ROPU and other published methods in terms of anticorrosive activity. The excellent anti-corrosive characteristic of the suggested nanocomposite coatings opens up new possibilities for the creation of advanced high-performance coatings for a variety of metal industries.

L-cysteine embedded core-shell ZnO microspheres composed of nanoclusters enhances anticancer activity against liver and breast cancer cells.

Nano-based products have become an apparent and effective option to treat liver cancer, which is a deadly disease, and minimize or eradicate these problems. The Core-shell ZnO microspheres composed of nanoclusters (ZnOMS-NCs) have shown that it is very worthwhile to administer the proliferation rate in HepG2 and MCF-7 cancer cells even at a very low concentration (5 µg/mL). ZnOMS-NCs were prepared through hydrothermal solution process and well characterized. The MTT assay revealed that the cytotoxic effects were dose-dependent (2.5 µg/mL-100 µg/mL) on ZnOMS-NCs. The diminished activity in cell viability induces the cytotoxicity response to the ZnOMS-NCs treatment of human cultured cells. The qPCR data showed that the cells (HepG2 and MCF-7) were exposed to ZnOMS-NCs and exhibited up-and downregulated mRNA expression of apoptotic and anti-apoptotic genes, respectively. In conclusion, flow cytometric data exhibited significant apoptosis induction in both cancer cell lines at low concentrations. The possible mechanism also describes the role of ZnOMS-NCs against cancer cells and their responses.

Neodymium oxide nanostructures and their cytotoxic evaluation in human cancer cells.

Neodymium oxide exhibits a unique property, which facilitates and largely utilized as an industrial applications. A number of cytotoxic study is available but very limited information is available to understand their biological activity with neodymium oxide at a very low conc- entration of the material. The present work was designed to understand the cytotoxicity against liver (HepG-2) and lung (A-549) cancer cells. Initially, Neodymium oxides (Nd2O3) were prepared and characterized with various instruments. The crystallinity and morphology of Nd2O3 powder were examined with instruments such as X-Ray Diffraction (XRD), scanning electron microscope (SEM), Transmission electron microscopy (TEM), Energy Dispersive X-Ray Analysis (EDX) respectively, revealed the size of curved nanostructure are ~140 ± 2 in diameter whereas length goes upto ~700 nm with elemental composition. The cytotoxicity study was conducted with MTT, NRU assay with genotoxicity study via ROS, cell cycle and qPCR analysis. The cells cytotoxic assessment were analysed via MTT(3-(4,5-Dimethylthiazol-2-yl)- 2,5-Diphenyl tetra zolium Bromide) and Neutral Red Uptake (NRU) assay with neodymium oxide (Nd2O3), which indicates the reduction in cell viability. Additionally, cell-cycle analysis showed an increase in the apoptotic peak after a 24-h. Quantitative real-time PCR (RT-PCR) data revealed that apoptotic genes such as p53, bax, and caspase-3 were up regulated, whereas bcl-2, an anti-apoptotic gene, was down regulated; therefore, apoptosis was mediated through ROS and genotoxicity pathways. The experiments of cytotoxicity was tested and concludes that the Nd2O3 express a moderate and dose dependent effect on cancer cells. The ROS, cell cycle analysis and qPCR showed that Nd2O3 exhibit the capability to cells death via ROS generation and genotoxicity study pathways.

The Role of Strontium in CeNiO3 Nano-Crystalline Perovskites for Greenhouse Gas Mitigation to Produce Syngas.

The transition metal-based catalysts for the elimination of greenhouse gases via methane reforming using carbon dioxide are directly or indirectly associated with their distinguishing characteristics such as well-dispersed metal nanoparticles, a higher number of reducible species, suitable metal-support interaction, and high specific surface area. This work presents the insight into catalytic performance as well as catalyst stability of CexSr1-xNiO3 (x = 0.6-1) nanocrystalline perovskites for the production of hydrogen via methane reforming using carbon dioxide. Strontium incorporation enhances specific surface area, the number of reducible species, and nickel dispersion. The catalytic performance results show that CeNiO3 demonstrated higher initial CH4 (54.3%) and CO2 (64.8%) conversions, which dropped down to 13.1 and 19.2% (CH4 conversions) and 26.3 and 32.5% (CO2 conversions) for Ce0.8Sr0.2NiO3 and Ce0.6Sr0.4NiO3, respectively. This drop in catalytic conversions post strontium addition is concomitant with strontium carbonate covering nickel active sites. Moreover, from the durability results, it is obvious that CeNiO3 exhibited deactivation, whereas no deactivation was observed for Ce0.8Sr0.2NiO3 and Ce0.6Sr0.4NiO3. Carbon deposition during the reaction is mainly responsible for catalyst deactivation, and this is further established by characterizing spent catalysts.

Strontium-Doped Nickel Oxide Nanoparticles: Synthesis, Characterization, and Cytotoxicity Study in Human Lung Cancer A549 Cells.

In this manuscript, the grown and annealed strontium-doped nickel oxide nanoparticles (SrNiONPs) were synthesized using a precipitation method with nickel nitrate and strontium nitrate as precursor agents with trisodium citrate. Various characterization techniques, including X-ray diffraction pattern (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier transform infrared spectroscopy (FTIR), UV-visible, and zeta sizer, were used to thoroughly examine the samples. The XRD pattern (21 nm) was used to calculate the size, phases, and crystallinity of the material (SrNiONPs). In addition to characterization, the material was tested for cytotoxicity in lung cancer cells (A549). The viability test in A549 cells was performed using [3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide] (MTT) and Neutral Red Uptake (NRU) assay with SrNiONPs concentration ranging from 1 to 100 µg/mL. According to the MTT and NRU data, the toxicity studies are dose-dependent. SrNiONPs also increased reactive oxygen species (ROS) and were involved in apoptosis (A549 cells). Furthermore, quantitative PCR (qPCR) data revealed that the mRNA levels of apoptotic genes marker like p53, bax, and caspase-3 were upregulated, whereas bcl-2, an anti-apoptotic gene, was downregulated. As a result, apoptosis was mediated by the p53, bax, caspase3, and bcl-2 pathways, implying a potential mechanism by which SrNiONPs mediate their toxicity.

Study on the Synthesis of ZnO Nanoparticles Using Azadirachta indica Extracts for the Fabrication of a Gas Sensor.

This paper compared the effects of A. indica plant proteins over chemical methods in the morphology of zinc oxide nanoparticles (ZnO NPs) prepared by a co-precipitation method, and ethanol sensing performance of prepared thin films deposited over a fluorene-doped tin oxide (FTO) bind glass substrate using spray pyrolysis technique. The average crystallite sizes and diameters of the grain-sized cluster ZnO NPs were 25 and (701.79 ± 176.21) nm for an undoped sample and 20 and (489.99 ± 112.96) nm for A. india dye-doped sample. The fourier transform infrared spectroscopy (FTIR) analysis confirmed the formation of the Zn-O bond at 450 cm-1, and also showed the presence of plant proteins due to A. indica dye extracts. ZnO NPs films exhibited good response (up to 51 and 72% for without and with A. indica dye-doped extracts, respectively) toward ethanol vapors with quick response-recovery characteristics at a temperature of 250 °C for undoped and 225 °C for A. indica dye-doped ZnO thin films. The interaction of A. indica dye extracts helps to decrease the operating temperature and increased the response and recovery rates of the sensor, which may be due to an increase in the specific surface area, resulting in adsorption of more oxygen and hence high response results.

Anticancer Potential of Biogenic Silver Nanoparticles: A Mechanistic Study.

The continuous loss of human life due to the paucity of effective drugs against different forms of cancer demands a better/noble therapeutic approach. One possible way could be the use of nanostructures-based treatment methods. In the current piece of work, we have synthesized silver nanoparticles (AgNPs) using plant (Heliotropiumbacciferum) extract using AgNO3 as starting materials. The size, shape, and structure of synthesized AgNPs were confirmed by various spectroscopy and microscopic techniques. The average size of biosynthesized AgNPs was found to be in the range of 15 nm. The anticancer potential of these AgNPs was evaluated by a battery of tests such as MTT, scratch, and comet assays in breast (MCF-7) and colorectal (HCT-116) cancer models. The toxicity of AgNPs towards cancer cells was confirmed by the expression pattern of apoptotic (p53, Bax, caspase-3) and antiapoptotic (BCl-2) genes by RT-PCR. The cell viability assay showed an IC50 value of 5.44 and 9.54 µg/mL for AgNPs in MCF-7 and HCT-116 cell lines respectively. We also observed cell migration inhibiting potential of AgNPs in a concentration-dependent manner in MCF-7 cell lines. A tremendous rise (150-250%) in the production of ROS was observed as a result of AgNPs treatment compared with control. Moreover, the RT-PCR results indicated the difference in expression levels of pro/antiapoptotic proteins in both cancer cells. All these results indicate that cell death observed by us is mediated by ROS production, which might have altered the cellular redox status. Collectively, we report the antimetastasis potential of biogenic synthesized AgNPs against breast and colorectal cancers. The biogenic synthesis of AgNPs seems to be a promising anticancer therapy with greater efficacy against the studied cell lines.

Dual role of oxidative stress-JNK activation in autophagy and apoptosis induced by nickel oxide nanoparticles in human cancer cells.

Nickel oxide nanoparticles (NiO-NPs) are an important group of nanoparticles with increasing applications in many aspects of industry. At present, there is evidence demonstrating the cytotoxic characteristics of NiO-NPs, while the involvement of autophagy in the cytotoxicity of NiO-NPs has not been reported. In this study, we aimed to study the role of autophagy in the cytotoxicity of NiO-NPs and the underlying regulatory mechanisms. First, we provided evidence that NiO-NPs induce autophagy in human cancer cells. Second, we found that the enhanced autophagic flux by NiO-NPs via the generation of intracellular reactive oxygen species (ROS) from mitochondria and the subsequent activation of the JNK pathway. Third, we demonstrated that the activation of JNK is a main force in mediating NiO-NPs-induced apoptosis. Finally, we demonstrated that the autophagic response plays an important protective role against the cytotoxic effect of NiO-NPs. Therefore, this study identifies the dual role of oxidative stress-JNK activation in the biological effects of NiO-NPs via promoting autophagy and mediating apoptosis. Understanding the protective role of autophagy and the underlying mechanism is important for the potential application of NiO-NPs in the biomedical industry.

Cytotoxicity and cell death induced by engineered nanostructures (quantum dots and nanoparticles) in human cell lines.

In recent years, the industrial use of ZnO quantum dots (QDs) and nanoparticles (NPs) has risen and there is a high chance of these nanoparticles affecting human health. In this study, different sizes of ZnO-NPs (6-100 nm) were prepared and characterized. The generation of reactive oxygen species (ROS) and its involvement in apoptosis when HepG2 cells were exposed to QDs (6 nm) and NPs of different sizes (15-20, 50, and 100 nm) was also investigated. At a concentration of 25-200 µg/mL, NPs induced dose-dependent cytotoxicity in HepG2 cells. The engineered NPs increased oxidative stress in a dose- and size-dependent manner, as seen by an increase in ROS production, lipid peroxidation, and glutathione reduction. Furthermore, cell-cycle analysis of HepG2 cells treated with different sizes of NPs showed an increase in the apoptotic peak after a 24-h exposure period. Quantitative real-time PCR data showed that the mRNA levels of apoptotic marker genes such as p53, bax, and caspase-3 were upregulated, whereas bcl-2, an anti-apoptotic gene, was downregulated; therefore, apoptosis was mediated through the p53, bax, caspase-3, and bcl-2 pathways, suggesting a possible mechanism by which QDs and NPs of ZnO mediate their toxicity.Graphic abstract.

Cold Atmospheric Plasma and Gold Quantum Dots Exert Dual Cytotoxicity Mediated by the Cell Receptor-Activated Apoptotic Pathway in Glioblastoma Cells.

Brain cancer malignancies represent an immense challenge for research and clinical oncology. Glioblastoma is the most lethal form of primary malignant brain cancer and is one of the most aggressive forms commonly associated with adverse prognosis and fatal outcome. Currently, combinations of inorganic and organic nanomaterials have been shown to improve survival rates through targeted drug delivery systems. In this study, we developed a dual treatment approach using cold atmospheric plasma (CAP) and gold quantum dots (AuQDs) for brain cancer. Our results showed that CAP and AuQDs induced dual cytotoxicity in brain cancer cells via Fas/TRAIL-mediated cell death receptor pathways. Moreover, combination treatment with CAP and AuQDs suppressed the motility and sphere-formation of brain cancer cells, which are recognized indicators of cancer aggressiveness. Taken together, the application of AuQDs can improve the efficiency of CAP against brain cancer cells, posing an excellent opportunity for advancing the treatment of aggressive glioblastomas.

Cymbopogon Citratus Functionalized Green Synthesis of CuO-Nanoparticles: Novel Prospects as Antibacterial and Antibiofilm Agents.

Chemically synthesized copper oxide nanoparticles (CuONPs) involve the generation of toxic products, which narrowed its biological application. Hence, we have developed a one-pot, green method for CuONP production employing the leaf extract of Cymbopogon citratus (CLE). Gas chromatography-mass spectrometry (GC-MS) analysis confirmed the capping of CuONPs by CLE esters (CLE-CuONPs). Fourier-transform infrared (FTIR) showed phenolics, sugars, and proteins mediated nucleation and stability of CLE-CuONPs. X-ray diffraction (XRD) and transmission electron microscopy (TEM) revealed CLE-CuONPs between 11.4 to 14.5 nm. Staphylococcus aureus-1 (MRSA-1), Staphylococcus aureus-2 (MSSA-2) exposed to CLE-CuONPs (1500 µg/mL) showed 51.4%, 32.41% survival, while Escherichia coli-336 (E. coli-336) exposed to 1000 µg/mL CLE-CuONPs showed 45.27% survival. Scanning electron microscopy (SEM) of CLE-CuONPs treated E. coli-336, MSSA-2 and MRSA-1 showed morphological deformations. The biofilm production by E. coli-336 and MRSA-1 also declined to 33.0 ± 3.2% and 49.0 ± 3.1% at 2000 µg/mL of CLE-CuONPs. Atomic absorption spectroscopy (AAS) showed 22.80 ± 2.6%, 19.2 ± 4.2%, and 16.2 ± 3.6% accumulation of Cu2+ in E. coli-336, MSSA-2, and MRSA-1. Overall, the data exhibited excellent antibacterial and antibiofilm efficacies of esters functionalized CLE-CuONPs, indicating its putative application as a novel nano-antibiotic against multi drug resistance (MDR) pathogenic clinical isolates.

Phorate triggers oxidative stress and mitochondrial dysfunction to enhance micronuclei generation and DNA damage in human lymphocytes.

Herein, we studied phorate for its toxicological effects in human lymphocytes. Phorate treatment for 3 h has induced significant increase in the lymphocytic DNA damage. Compared to control, comet data from highest concentration of phorate (1000 µM) showed 8.03-fold increase in the Olive tail moment (OTM). Cytokinesis blocked micronucleus (CBMN) assay revealed 6.4-fold increase in binucleated micronucleated (BNMN) cells following the exposure with phorate (200 µM) for 24 h. The nuclear division index (NDI) in phorate (200 µM) treated cells reduced to 1.8 vis-à-vis control cells showed NDI of 1.94. Comparative to untreated control, 60.43% greater DCF fluorescence was quantitated in lymphocytes treated with phorate (500 µM), affirming reactive oxygen species (ROS) generation and oxidative stress. Flow cytometric data of phorate (200 µM) treated lymphocytes showed 81.77% decline in the fluorescence of rhodamine 123 (Rh123) dye, confirming the perturbation of mitochondrial membrane potential (ΔΨm). Calf thymus DNA (ct-DNA) treated with phorate (1000 µM) exhibited 2.3-fold higher 8-Hydroxy-2'-deoxyguanosine (8-oxodG) DNA adduct formation, signified the oxidative DNA damage. The alkaline unwinding assay revealed 4.0 and 6.5 ct-DNA strand breaks when treated to phorate and phorate-Cu (II) complex. Overall, the data unequivocally suggests the cyto- and genotoxic potential of phorate in human lymphocytes, which may induce comparable toxicological consequences in persons occupationally or non-occupationally exposed to insecticide phorate.

Organophosphorus flame retardant (tricresyl phosphate) trigger apoptosis in HepG2 cells: Transcriptomic evidence on activation of human cancer pathways.

Tricresyl phosphate (TCP) is one of the organophosphorus flame retardants (OPFRs) used as plasticizer in consumer products and mixed as a lubricant in commercial jet engine oil, reportedly induce neurotoxicity and aerodynamic syndrome. No studies have been attempted so far on TCP to induce hepatotoxicity in human cells. This study for the first time confirms the hepatotoxic potential and activation of cancer pathways in TCP treated human hepatocellular cells (HepG2). MTT and NRU data showed 39.3% and 49.85% decline in HepG2 survival when exposed to the highest concentration of TCP (400 µM) for 3 days. Comet assay showed 27.1-fold greater DNA damage in cells treated with TCP (400 µM). Flow cytometric analysis revealed an upsurge in the intracellular reactive oxygen species (ROS) and nitric oxide (NO) production in cells, affirming oxidative stress. TCP (400 µM) exposure resulted in 27% reduction in Rh123 fluorescence, indicating dysfunction of mitochondrial membrane potential (ΔΨm). Cell cycle analysis exhibited 62.53% cells in the subG1 apoptotic phase after TCP (400 µM) treatment, also a massive increase in Ca2+ influx validate the on-set of apoptosis in cells. Immunofluorescence of TCP exposed cells showed activation of p53, caspase3, caspase9 reaffirming the involvement of mitochondrial-dependent intrinsic apoptotic signaling. qPCR array of 84 genes unravel the transcriptomic alterations in HepG2 cells after TCP treatment. mRNA transcripts of ATP5A1, GADD45A, IGFBP5, SOD1, STMN1 genes were prominently upregulated providing candid evidence on TCP mediated activation of human cancer pathways to orchestrate the apoptotic death of HepG2 cells, specifying hepatotoxic potential of TCP.

Cold atmospheric plasma and silymarin nanoemulsion synergistically inhibits human melanoma tumorigenesis via targeting HGF/c-MET downstream pathway.

BACKGROUND: Recent studies claimed the important role of cold atmospheric plasma (CAP) with nanotechnology in cancer treatments. In this study, silymarin nanoemulsion (SN) was used along with air CAP as therapeutic agent to counter human melanoma. METHODS: In this study, we examined the combined treatment of CAP and SN on G-361 human melanoma cells by evaluating cellular toxicity levels, reactive oxygen and nitrogen species (RONS) levels, DNA damage, melanoma-specific markers, apoptosis, caspases and poly ADP-ribose polymerase-1 (PARP-1) levels using flow cytometer. Dual-treatment effects on the epithelial-mesenchymal transition (EMT), Hepatocyte growth factor (HGF/c-MET) pathway, sphere formation and the reversal of EMT were also assessed using western blotting and microscopy respectively. SN and plasma-activated medium (PAM) were applied on tumor growth and body weight and melanoma-specific markers and the mesenchymal markers in the tumor xenograft nude mice model were checked. RESULTS: Co-treatment of SN and air CAP increased the cellular toxicity in a time-dependent manner and shows maximum toxicity at 200 nM in 24 h. Intracellular RONS showed significant generation of ROS (< 3 times) and RNS (< 2.5 times) in dual-treated samples compared to control. DNA damage studies were assessed by estimating the level of γ-H2AX (1.8 times), PD-1 (> 2 times) and DNMT and showed damage in G-361 cells. Increase in Caspase 8,9,3/7 (> 1.5 times), PARP level (2.5 times) and apoptotic genes level were also observed in dual treated group and hence blocking HGF/c-MET pathway. Decrease in EMT markers (E-cadherin, YKL-40, N-cadherin, SNAI1) were seen with simultaneously decline in melanoma cells (BRAF, NAMPT) and stem cells (CD133, ABCB5) markers. In vivo results showed significant reduction in SN with PAM with reduction in tumor weight and size. CONCLUSIONS: The use of air CAP using µ-DBD and the SN can minimize the malignancy effects of melanoma cells by describing HGF/c-MET molecular mechanism of acting on G-361 human melanoma cells and in mice xenografts, possibly leading to suitable targets for innovative anti-melanoma approaches in the future.

Gold quantum dots impair the tumorigenic potential of glioma stem-like cells via ß-catenin downregulation in vitro.

BACKGROUND: Over the past several decades, the incidence of solid cancers has rapidly increased worldwide. Successful removal of tumor-initiating cells within tumors is essential in the field of cancer therapeutics to improve patient disease-free survival rates. The biocompatible multivarient-sized gold nanoparticles (MVS-GNPs) from quantum dots (QDs, <10 nm) to nanosized (up to 50 nm) particles have vast applications in various biomedical areas including cancer treatment. The role of MVS-GNPs for inhibition of tumorigenic potential and stemness of glioma was investigated in this study. METHODS: Herein, MVS-GNPs synthesized and characterized by means of X-ray diffraction pattern (XRD) and transmission electron microscopy (TEM) techniques. Afterwards, interaction of these GNPs with glioma stem-cell like cells along with cancer cells were evaluated by MTT, cell motility, self-renewal assays and biostatistics was also applied. RESULTS: Among these GNPs, G-QDs contributed to reduce metastatic events and spheroid cell growth, potentially blocking the self-renewal ability of these cells. This study also uncovers the previously unknown role of the inhibition of CTNNB1 signaling as a novel candidate to decrease the tumorigenesis of glioma spheroids and subsequent spheroid growth. The accurate and precise biostatistics results were obtained at quantify level. CONCLUSION: In summary, G-QDs may exhibit possible contribution on suppressing the growth of tumor-initiating cells. These data reveal a unique therapeutic approach for the elimination of residual resistant stem-like cells during cancer treatment.

Microwave plasma-assisted silicon nanoparticles: cytotoxic, molecular, and numerical responses against cancer cells.

Silicon nanoparticles (SiNPs), which have a special place in material science due to their strong luminescent property and wide applicability in various physicochemical arenas, such as solar cells and LEDs, were synthesised by a microwave plasma-assisted process using an argon-silane mixture. Several characterization tools were applied to check the crystallinity (XRD) and morphological (FESEM, TEM, ∼20 ± 2 nm size) and topographical (AFM, ∼20 nm) details of the NPs. The high-purity SiNPs were applied on myoblast cancer cells to investigate the reactivity of the NPs at different doses (200, 1000 and 2000 ng mL-1) for different incubation periods (24 h, 48 h & 72 h). The MTT assay was utilized to determine the percentage of viable and non-viable cells, while the cell organization was observed via microscopy and CLSM. Additionally, the molecular responses (RT-PCR), such as apoptosis, were analyzed in presence of caspase 3 and 7, and the results showed an upregulation with SiNPs. To validate the obtained data, analytical studies were also performed for the SiNPs via statistical analysis and the most reliable data values were evaluated and acceptable as per the ICH guidelines.

Anticancer Potential of Green Synthesized Silver Nanoparticles Using Extract of Nepeta deflersiana against Human Cervical Cancer Cells (HeLA).

In this study, silver nanoparticles (AgNPs) were synthesized using aqueous extract of Nepeta deflersiana plant. The prepared AgNPs (ND-AgNPs) were examined by ultraviolet-visible spectroscopy, Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), transmission electron microscopy (TEM), scanning electron microscope (SEM), and energy dispersive spectroscopy (EDX). The results obtained from various characterizations revealed that average size of synthesized AgNPs was 33 nm and in face-centered-cubic structure. The anticancer potential of ND-AgNPs was investigated against human cervical cancer cells (HeLa). The cytotoxic response was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), neutral red uptake (NRU) assays, and morphological changes. Further, the influence of cytotoxic concentrations of ND-AgNPs on oxidative stress markers, reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest and apoptosis/necrosis was studied. The cytotoxic response observed was in a concentration-dependent manner. Furthermore, the results also showed a significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels. The cell cycle analysis and apoptosis/necrosis assay data exhibited ND-AgNPs-induced SubG1 arrest and apoptotic/necrotic cell death. The biosynthesized AgNPs-induced cell death in HeLA cells suggested the anticancer potential of ND-AgNPs. Therefore, they may be used to treat the cervical cancer cells.