Cell Line MG-63 Research Articles

α,γ-Diketocarboxylic Acids and Their Esters Act as Carbonic Anhydrase IX and XII Selective Inhibitors.

Among human carbonic anhydrase (CA) inhibitors, the α,γ-diketocarboxylic acids and esters are still poorly investigated. Here, we report the first compounds of this class (1-6) acting as potent inhibitors at low nanomolar level against the cancer-related human CA IX and XII, and 2-3 magnitude orders selective toward the cytosolic isoforms hCA I and II. At enzymatic level, the α,γ-diketoacids 1-3 were more effective inhibitors compared to the corresponding ethyl esters 4-6. The phenyl- and α-naphthyl-containing compounds (1, 3, 4, and 6) behaved as dual hCA IX/XII inhibitors, while the β-naphthyl analogues (2 and 5) exhibited hCA IX-selective inhibition. In MG63 and HOS osteosarcoma (OS) cell lines, the ethyl esters 5 and 6 displayed dose-dependent reduction of viability and proliferation after 72 h treatment, with 6 being more potent than 5 likely for its dual hCA IX/XII inhibition.

DDX10 overexpression predicts worse prognosis in osteosarcoma and its deletion prohibits cell activities modulated by MAPK pathway

Osteosarcoma (OS) is an invasive cancer in the skeletal system. The molecular mechanism of its etiology and pathogenesis are still not clear, so the effective treatment strategy of OS needs further research. First, we analyzed the expression level and prognostic ability of the RNA helicase DDX10 in OS patients based on the data obtained from GEO database. Next, we used CCK8 to test OS cell viability. Besides, we used wound-healing assay and transwell migration assay to detect cell migration of OS MG63 cell line. And the cell invasion was tested by transwell invasion assay. Moreover, we used QRT-PCR and western blot to analyze the mRNA and protein expression levels. We found that DDX10 was significantly over-expressed in OS patients and elevated level of DDX10 was associated with a poor prognosis. Silencing of DDX10 inhibited proliferation, invasion and migration of MG63 cells in vitro. Down-regulation of DDX10 inhibited MAPK signaling pathway. The expression of p-MEK and p-ERK were also decreased by silencing of DDX10. Therefore, Silencing of DDX10 inhibited proliferation, invasion and migration of MG63 cells, which might be regulated by suppression of MAPK pathway. In conclusion, our results unfold a novel area of studying for understanding how DDX10 functions in OS oncogenic and prognostic significance, accordingly implying a promising therapeutic target for OS treatment.

Impact of transition metal ions on the structure and bioactivity of alkali-free bioactive glasses

Transition metal ions are essential micronutrients for all living organisms and play an important role in bone metabolism. In the present study, we investigated the impact of transition metal ions (Cu, Co, Mn, Fe) on the structure and bioactivity of bioactive glasses. The emphasis was laid on understanding their influence on the chemical dissolution behavior of glasses and its impact on their vitro bioactivity, osteoblast proliferation and oxidative stress levels. The structure of glasses was studied by using molecular EXAFS in combination with Raman spectroscopy. The apatite-forming ability of glasses has been investigated by X-ray diffraction, infrared spectroscopy after immersion of glass powders in simulated body fluid (SBF) for time durations varying between 1 and 7 days. A significant effect on the bioactivity was observed with addition of transition metal ions. The cellular responses were observed in vitro on glass powders using human osteosarcoma MG63 cell line. The dose-dependent cytoprotective effect of glasses with respect to the concentration of transition metal ions (Cu, Co, Mn, Fe) released from the glasses is also discussed.

Network Pharmacology Integrated Molecular Docking Reveals the Antiosteosarcoma Mechanism of Biochanin A.

Background As the malignant tumor with the highest incidence in teenagers, osteosarcoma has become a major problem in oncology research. In addition to surgical management, the pharmacotherapeutic strategy for osteosarcoma treatment is an attractive way to explore. It has been demonstrated that biochanin A has an antitumor capacity on multiple kinds of solid tumor, including osteosarcoma. But the precise mechanism of biochanin A against osteosarcoma is still needed to be discovered. Objective To identify the potential therapeutic targets of biochanin A in treating osteosarcoma. Methods In present study, an integrated approach including network pharmacology and molecular docking technique was conducted, which mainly comprises target prediction, network construction, gene ontology, and pathway enrichment. CCK8 test was employed to evaluate the cell viability of MG63 cells. Western-blot was used to verify the target proteins of biochanin A. Results Ninety-six and 114 proteins were obtained as the targets of biochanin A and osteosarcoma, respectively. TP53, IGF1, JUN, BGLAP, ATM, MAPK1, ATF3, H2AFX, BAX, CDKN2A, and EGF were identified as the potential targets of biochanin A against osteosarcoma. Based on the western-blot detection, the expression of BGLAP, BAX, and ATF3 in MG63 cell line changed under the treatment of biochanin A. Conclusion Biochanin A can effectively suppress the proliferation of osteosarcoma and regulate the expression of BGLAP, BAX, and ATF3, which may act as the potential therapeutic targets of osteosarcoma.

Silver derivatives of multi-donor heterocyclic thioamides as antimicrobial/anticancer agents: unusual bio-activity against methicillin resistant S. aureus, S. epidermidis, and E. faecalis and human bone cancer MG63 cell line.

The basic aim of this study pertains to the synthesis of silver nitrate complexes and the study of their antimicrobial and anticancer bio-activity. A series of new silver(i) derivatives of N-substituted-imidazolidine-2-thiones (L-NR, R = Et, Prn, Bun, Ph), purine-6-thione (purSH2), 2-thiouracil (tucH2), pyrimidine-2-thione (pymSH) and pyridine-2-thione (pySH) of composition [Ag(S-L-NR)(PPh3)2(ONO2)] {R = Et (1), Prn (2), Bun (3), Ph (4)}, [Ag2(N,S-purSH2)2(μ-dppm)2](NO3)2·2H2O (5) (dppm = Ph2P–CH2–PPh2), [Ag(L)(PPh3)2](NO3) {L = N,S-purSH2 (6); S-tucH2 (7)}, [Ag(N,S-pymS)(PPh3)2](CH3OH) (8), and [Ag(N,S-pyS)(PPh3)2] (9) have been synthesized and structurally characterized. These new and some previously reported complexes {[Ag2(L-NH)4(PPh3)2](NO3)2 (10), [Ag(L-NMe)2(PPh3)](NO3) (11), and [Ag(S-bzimSH)2(PPh3)2](OAc) (12), L-NH = 1,3-imidazolidine-2-thione; L-NMe = 1-methyl-3-imidazolidine-2-thione and bzimSH2 = benzimidazoline-2-thione)} have shown moderate to high anti-microbial activity against Gram positive bacteria, namely methicillin resistant Staphylococcus aureus (MRSA) and Staphylococcus aureus (MTCC 740), and Gram negative bacteria, namely Staphylococcus epidermidis (MTCC 435), Enterococcus faecalis (MTCC 439), Shigella flexneri (MTCC 1457) and a yeast Candida albicans (MTCC 22). These complexes have also been found to be bio-safe as studied using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. The anti-tumor study of silver complexes against human osteosarcoma cell line (MG63) has shown IC50 values in the range of 6–33 μM.

MicroRNA-221 regulates osteosarcoma cell proliferation, apoptosis, migration, and invasion by targeting CDKN1B/p27.

MicroRNAs (miRNAs, miR) are of critical importance in growth and metastasis of cancer cells; however, the underlying functions of miRNAs in osteosarcoma (OS) remain largely unknown. This study was aimed to elucidate the role of miR-221 in regulating the biological behavior of OS cells. The proliferation ability was examined by cell counting kit-8 (CCK-8) and cell cycle assay. The abilities of cell migration, invasion, and apoptosis were monitored by transwell assay and flow cytometry, respectively. The effect of miR-221 on cyclin-dependent kinase inhibitor 1B (CDKN1B) expression was evaluated by luciferase assays, real-time polymerase chain reaction, and Western blot analysis. We found that miR-221 was elevated in OS cell lines compared with the normal osteoblastic cell line. Transfection of the miR-221 inhibitor into MG63 and U-2OS cell lines obviously suppressed cell proliferation, migration, and invasion, which is accompanied with cell cycle arrest in G0/G1 phase. Furthermore, luciferase reporter assays indicated that CDKN1B is directly targeted by miR-221 in OS cells. Knockdown of CDKN1B inhibited the effects of miR-221 inhibitor, along with decreased Bax and caspase-3 and increased cyclin E, cyclin D1, Bcl-2, Snail, and Twist1 expression. The results suggested that miR-221 might act as a potentially useful target for treatment of OS.

Synergic effect of CNT and mechanical loading for acceleration of cell differentiation

Herein, we investigate the synergic effect of carbon nanotubes (CNT) in conjunction with mechanical load applied in early stage of cell cultivation to accelerate differentiation in bone cells. To improve their biofunctionality, CNT were functionalized with carboxyl groups and RGD peptide. The effect of CNT functionalization on cell proliferation and formation of cell aggregates with hastened production of calcium deposits was studied with and MG63 cell lines in static and dynamic conditions. Combination of CNT with mechanical load promoted significantly higher osteogenic marker expression and formation of calcium deposits in comparison to the control, particularly in case of MSC.

MiR-503 is down-regulated in osteosarcoma and suppressed MG63 proliferation and invasion by targeting VEGFA/Rictor.

We analyzed the expression of miR-503 in osteosarcoma tissues (OS) and discussed the clinical significance of our findings. To provide a theoretical basis for clinical applications, prognosis prediction and treatment of osteosarcoma, we studied the biological function of miR-503 and its mechanism in MG63 osteosarcoma cells. Real-time polymerase chain reaction (PCR) was used to detect the expression of miR-503 in 45OS tissues and 20osteochondroma tumors, analyzing the relationship between clinical pathology and follow-up data. Cox multivariate analysis revealed the clinical and pathological features of the osteosarcoma index and the influence of miR-503 expression on OS prognosis. To observe the effect on cell proliferation and invasion, MG-63 cells were transfected with miR-503. The TargetScan and PicTar bioinformatics method was used to analyze the probable target gene of miR-503 and, combined with the function of the target genes, resulted in a final validation of related pathways. miR-503 was significantly down-regulated in primary OS samples (26/45, 57.8%). The median miR-503 expression level in osteosarcoma was two-fold lower than that in osteochondroma (median expression 6.4 and 13.09, respectively, P< 0.05). The less-expressed miR-503 was associated with Enneking stage (p= 0.004) and invasion (p= 0.015) of OC. Patients with low miR-503 expression had poorer overall survival time. In the multivariate analysis, miR-503 was a significant prognostic factor (P= 0.010). miR-503 can inhibit proliferation and invasion in the MG63 cell line. Using bioinformatics, VEGFA and Rictor were determined to be the likely downstream target genes of miR-503. VEGFA, Rictor, Akt and Erk1/2 were negatively regulated by the overexpression of miR-503. In conclusion, miR-503 has significant tumor-suppressor biological activity and is thus likely to become a new target for the treatment of osteosarcoma.

MicroRNA-885-5p promotes osteosarcoma proliferation and migration by downregulation of cell division cycle protein 73 homolog expression.

Osteosarcoma (OS) is the most common primary malignant bone tumor. Numerous studies have strongly implicated the ectopic expression of microRNAs (miRNAs/miRs), including miR-885-5p, which is aberrantly expressed in several cancer types, in multiple cancer-related processes. However, the role of miR-885-5p in OS remains unknown. In the present study, it was found that the expression of miR-885-5p was markedly upregulated in OS cell lines and clinical tissues. Moreover, high expression of miR-885-5p was significantly associated with the development of OS. The human OS MG-63 cell line was transfected with recombinant lentivirus to regulate miR-885-5p expression. Overexpressed miR-885-5p significantly promoted the proliferation and migration of MG-63 cells in vitro, while downregulating miR-885-5p expression reversed these effects. Furthermore, bioinformatic analysis was used to predict the potential target genes of miR-885-5p, and cell division cycle protein 73 homolog (CDC73) was identified as a novel and direct target of miR-885-5p. This interaction was further confirmed using reverse transcription-quantitative polymerase chain reaction, western blotting and luciferase activity assays. These findings suggest that miR-885-5p serves a critical role in facilitating OS proliferation and migration, and can regulate CDC73 expression in OS cells and tissues. Thus, miR-885-5p could be a promising novel therapeutic biomarker for OS.

TUFT1 promotes osteosarcoma cell proliferation and predicts poor prognosis in osteosarcoma patients

ObjectiveThis study is aimed at exploring the role of TUFT1 in osteosarcomas.MethodsWe investigated the expression of TUFT1 in osteosarcoma cell lines and explored the correlation between TUFT1 expression and prognosis in osteosarcoma patients based on the expression data downloaded from Gene Expression Omnibus (GEO) website. The effects of TUFT1 on osteosarcoma cell proliferation, migration and invasion were investigated by silencing TUFT1 in osteosarcoma MG63 cell line. Finally, western blot was performed to determine the expression changes of MAPK signaling pathway related proteins after silencing TUFT1.ResultsWe found that the expression of TUFT1 was significantly up-regulated in osteosarcoma cell lines compared with the normal control. Using Kaplan-Meier analysis, we identified that high TUFT1 expression was positively correlated with poor prognosis in osteosarcoma patients. Furthermore, knockdown of TUFT1 remarkably inhibited MG63 cell proliferation, migration and invasion. Using western blot analysis, we found that the phosphorylation levels of MEK and ERK were reduced obviously in MG63 cells after silencing TUFT1 (p<0.01).ConclusionsOur results demonstrated that TUFT1 plays a promoting role in MG63 cell proliferation and metastasis and has the potential to be a predictor as well as a therapeutic target for osteosarcoma patients.

MiR-155 affects osteosarcoma cell proliferation and invasion through regulating NF-κB signaling pathway.

Osteosarcoma can form tumor osteoid tissue and bone tissue directly or indirectly through cartilage stage. It mainly occurs in children and adolescents with high mortality. MicroRNA (miRNA) possesses tissue sensitivity as tumor biomarker and plays a promoting or inhibitory role in tumor pathogenesis as oncogene or tumor suppressor gene. It was found that miR-155 was abnormally expressed in tumor and could be treated as a biomarker for cancer progression. However, miR-155 expression in osteosarcoma and related mechanism still remains unclear. This study aimed to explore the role of miR-155 in osteosarcoma occurrence and development. Osteosarcoma cell line MG-63 was cultured in vitro and transfected by miR-155 mimics or inhibitor. MiR-155 expression was examined by Real-time PCR (RT-PCR). Cell proliferation was evaluated by MTT assay. Caspase 3 activity was determined by caspase 3 activity detection kit. Cell invasion was measured by transwell assay. B-cell lymphoma-2 (Bcl-2) and nuclear factor κB (NF-κB) protein expressions were assessed by Western blot. MiR-155 mimics significantly up-regulated miR-155 expression, promoted MG-63 cell proliferation and invasion, inhibited caspase 3 activity, and up-regulated expressions of NF-κB and Bcl-2 compared with control group (p < 0.05). However, miR-155 inhibitor significantly inhibited MG-63 cell proliferation and invasion, enhanced caspase 3 activity, and reduced expressions of NF-κB and Bcl-2 compared with control group (p < 0.05). MiR-155 affected osteosarcoma cell proliferation and apoptosis through regulating NF-κB signaling pathway, indicating it might be a new biomarker for osteosarcoma diagnosis and treatment.

Mg0.5Ni0.5Fe2O4 nanoparticles as heating agents for hyperthermia treatment

AbstractIn the present work, Mg0.5Ni0.5Fe2O4 nanopowders were prepared by a sol‐gel combustion method. The magnetic properties, heat generation ability in an AC magnetic field and cytotoxicity of the mixed ferrite nanopowders were investigated. The results showed that the powders have crystalline spinel structure with a particle size in the range of 20‐90 nm. Maximum saturation magnetization (Ms) of 51 emu/g was obtained for the Mg0.5Ni0.5Fe2O4 nanoparticles calcined at 900°C. The results showed that, the coercivity (Hc) of the Mg0.5Ni0.5Fe2O4 initially increases up to 700°C and then decreases with increasing temperature, whereas the Ms of the samples continuously increases. The Mg0.5Ni0.5Fe2O4 sample exhibited a temperature increase up to 45°C during 10 minutes in the exposure of magnetic field of 200 Oe. By increasing the viscosity of ferrofluid, the heat generation ability of nanoparticles reduced up to 9% at magnetic field of 200 Oe. Cell compatibility of the ferrite powders was studied by MTT assay using MG63 cell line proliferation. MTT results showed that calcination temperature of the Mg0.5Ni0.5Fe2O4 nanoparticles significantly affects the cell compatibility.

Silencing of miR-19a-3p enhances osteosarcoma cells chemosensitivity by elevating the expression of tumor suppressor PTEN.

MicroRNAs (miRNAs/miRs) are small non-coding RNAs, which serve important roles in tumor progression. The present study analyzed the role of miR-19a-3p in the chemosensitivity of osteosarcoma (OS) cells. Overexpression of miR-19a-3p was observed in OS cells and a cisplatin-resistant MG63 cell line was subsequently constructed. It was observed that miR-19a-3p inhibitor transfection suppressed cell proliferation and decreased the expression of Ki67 and PCNA compared with the cisplatin treatment group. miR-19a-3p inhibitor transfection also promoted apoptotic rate, increased the expression of Bcl-2 associated X, apoptosis regulator (Bax) and markedly decreased the expression of Bcl-2 compared with the cisplatin treatment group. These results elucidated that silencing of miR-19a-3p enhanced chemosensitivity of OS cells to Cisplatin, through suppressing cell proliferation and promoting cell apoptosis during treatment with Cisplatin. Bioinformatics study and luciferase reporter assays indicated that PTEN was a target of miR-19a-3p, and western blotting demonstrated that PTEN expression was negatively regulated by miR-19a-3p in OS cells. In addition, overexpression of PTEN decreased cell proliferation, but increased apoptotic rate compared with the cisplatin treatment group. It was observed that inhibition of PTEN by BpV(HOpic) upregulated cell proliferation and downregulated apoptotic rate compared with the Cisplatin-treated miR-19a-3p inhibitor group, indicating that inhibition of PTEN expression counteracted the effect of the miR-19a-3p inhibitor on the regulation of chemosensitivity in OS cells. Taken together, overexpression of miR-19a-3p was observed in OS cell lines and that downregulation of miR-19a-3p enhanced the chemosensitivity of OS cells to Cisplatin, by elevating the expression of the tumor suppressor, PTEN.

Matrix stiffness regulates epithelial-mesenchymal transition via cytoskeletal remodeling and MRTF-A translocation in osteosarcoma cells

Matrix stiffness is known to alter cellular behaviors in various biological contexts. Previous investigations have shown that epithelial–mesenchymal transition (EMT) promotes the progression and invasion of tumor. Mechanical signaling is identified as a regulator of EMT. However, the molecular mechanisms underlying the influence exerted by matrix stiffness on EMT in osteosarcoma remains largely unknown. Using polyacrylamide hydrogel model, we investigate the effects of matrix stiffness on EMT and migration in osteosarcoma. Our data indicates that high matrix stiffness regulates cell morphology and promotes EMT and migration in osteosarcoma MG63 cell line in vitro. Notably, matrix stiffness promotes polymerization of actin and nuclear accumulation of myocardin-related transcription factor A (MRTF-A). Furthermore, inhibiting MRTF-A by CCG 203971 significantly reduces EMT and migration on rigid gels. These data suggest that matrix stiffness of the tumor microenvironment actively regulate osteosarcoma EMT and migration through cytoskeletal remodeling and translocation of MRTF-A, which may contribute to cancer progression.

Effect of carbon nanotubes on in vitro cellular responses for bioglass application

Composite materials have been widely used in the field of biomedical science. In this study, the optimal concentration of bioglass/carbon nanotubes (BG/CNTs) in a composite powder was investigated. The composite was produced using the sol-gel process. When CNTs were added, they provided a crystal nucleation site for BG nanoparticles and decreased the heat treatment temperature required (from 700 °C to 500 °C). Compared to the BG group, a suitable quantity of CNTs increased the pore size (12.67 nm) of the composite materials. Meanwhile, the BG/0.05 CNT group showed weight gain results and revealed a faster apatite formation rate after 3 days than other composites. The apatite layer (which increased in thickness from 1.69 μm to 12.51 μm) was observed using scanning electron microscopy after 7 days. Additionally, the proliferation of the MG63 cell line showed an excellent performance with some BG/CNT ratios. It should be noted, however, that an excessive number (>0.05 wt%) of CNTs as filler in a BG matrix reduces cell growth.

Coining attributes of ultra-low concentration graphene oxide and spermine: An approach for high strength, anti-microbial and osteoconductive nanohybrid scaffold for bone tissue regeneration

Lack of auto osteogenesis and clinical complexities of repairing of bone after severe injuries, urge to develop a significant approach to promote regeneration of bone. The present work represents ornamentation of 2D rod-like nanohydroxyapatite (nHA) on ultra-low concentration graphene oxide (GO) sheet. The nanohybrids (GO-nHA) were incorporated into the spermine based high strength thermoplastic polyurethane-urea (PUU) matrices by in situ technique and the porous scaffolds were fabricated. 1 wt% GO-nHA filled scaffold displayed dramatically improved physico-mechanical properties. Cytotoxicity study using osteoblast cell like MG-63 cell line revealed positive cell viability (above 95%) and increased proliferation over a period of 14 days of culture. Semi-quantitative Real Time polymerase Chain Reaction (qRT-PCR) showed positive expression of collagen type I and osteocalcin indicating excellent maturation and biomineralization of osteoblasts. To avoid burden of carbonaceous particulate in body, very low percentage of GO (0.15%) was incorporated into the scaffold to improve mechanical properties, surface wettability, cell viability and cell proliferation drastically. Furthermore, in vivo study confirmed the promoted osteogenesis of PUU/GO-nHA scaffold in vivo without any cytotoxicity. Based on mechanical, in vitro and in vivo study the high strength nanohybrid scaffold exhibited tremendous potential for orthopedic applications.

Panobinostat mediated cell death: a novel therapeutic approach for osteosarcoma.

Osteosarcoma is an aggressive cancer with a poor long term prognosis. Neo-adjuvant poly-chemotherapy followed by surgical resection remains the standard treatment, which is restricted by multi-drug resistance. If first-line therapy fails, disease control and patient survival rate drop dramatically. We aimed to identify alternative apoptotic mechanisms induced by the histone deacetylase inhibitor panobinostat in osteosarcoma cells.Saos-2, MG63 and U2-OS osteosarcoma cell lines, the immortalized human osteoblast line hFOB and the mouse embryo osteoblasts (MC3T3-E1) were treated with panobinostat. Real time viability and FACS confirmed the cytotoxicity of panobinostat. Cell stress/death related factors were analysed by RT-qPCR and western blot. Cell morphology was assessed by electron microscopy.10 nM panobinostat caused cell viability arrest and death in all osteosarcoma and osteoblast cells. P21 up-regulation was observed in osteosarcoma cells, while over-expression of p73 was restricted to Saos-2 (TP53−/−).Survivin and Bcl-2 were suppressed by panobinostat. Endoplasmic reticulum (ER) stress markers BiP, CHOP, ATF4 and ATF6 were induced in osteosarcoma cells. The un-spliced Xbp was no further detectable after treatment.Autophagy players Beclin1, Map1LC3B and UVRAG transcripts over-expressed after 6 hours. Protein levels of Beclin1, Map1LC3B and p62 were up-regulated at 72 hours. DRAM1 was stable. Electron micrographs revealed the fragmentation and the disappearance of the ER and the statistically significant increase of autophagosome vesiculation after treatment.Panobinostat showed a synergistic suppression of survival and promotion of cell death in osteosarcoma cells. Panobinostat offers new perspectives for the treatment of osteosarcoma and other malignant bone tumours.

Adenovirus-mediated small interfering RNA targeting ezrin induces apoptosis and inhibits metastasis of human osteosarcoma MG-63 cells.

Osteosarcoma is a disease prone to recurrence and metastasis, and adenovirus expression vector is frequently studied as a therapeutic target of osteosarcoma in recent years. The present study attempts to explore the effect of adenovirus-mediated siRNA targetting ezrin on the proliferation, migration, invasion, and apoptosis of human osteosarcoma MG-63 cells. Human osteosarcoma MG-63 cell line was selected for construction of recombinant adenovirus vector. The mRNA and protein levels of ezrin, Bcl2-associated X protein (Bax), B cell lymphoma-2 (Bcl-2), p21, p53, Caspase-3, matrix metalloproteinase (MMP) 2 (MMP-2) and MMP-9, Cyclin D1, and cyclin-dependent kinase 4a (CDK4a) were determined. Through ELISA, the levels of Caspase-3, MMP-2 and MMP-9 were examined. Finally, human osteosarcoma MG-63 cell viability, growth, invasion, migration, and apoptosis were detected. Initially, adenovirus expression vector of ezrin was constructed by ezrin 2 siRNA sequence. Adenovirus-mediated siRNA targetting ezrin reduced expression of ezrin in MG-63 cells. The results revealed that adenovirus-mediated siRNA targetting ezrin elevated expression levels of Bax, p21, p53, and Caspase-3, Cyclin D1, and CDK4a and reduced expression levels of Bcl-2, MMP-2 and MMP-9. Furthermore, adenovirus-mediated siRNA targetting ezrin inhibited human osteosarcoma MG-63 cell viability, growth, invasion, and migration, and promoted apoptosis. Our study demonstrates that adenovirus-mediated siRNA targetting ezrin can induce apoptosis and inhibit the proliferation, migration, and invasion of human osteosarcoma MG-63 cells.

Phytosynthesis of gold nanoparticles: Characterization, biocompatibility, and evaluation of its osteoinductive potential for application in implant dentistry

Gold nanoparticles have been extensively used in diagnostics, biomedical imaging, and drug delivery owing to simple method of synthesis and versatile surface functionalization. Present investigation aims to evaluate the osteoinductive property of Salacia chinensis (SC) mediated gold nanoparticles (GNPs) for its application in implant dentistry. The formation of GNPs was assessed initially using the visual method and characterized analytically by using UV–visible spectroscopy, Zetasizer, X-RD, ICP-AES, AFM, and TEM. Green synthesized GNPs exhibited a remarkable stability in various blood components (0.2 M histidine, 0.2 M cysteine 2% bovine serum albumin, and 2% human serum albumin) and were found to be nontoxic when evaluated for their cytocompatibility and blood compatibility using periodontal fibroblasts and erythrocytes respectively. Exposure of GNPs to MG-63 cell lines displayed increased percent cell viability (138 ± 27.4) compared to the control group (96 ± 3.7) which confirms its osteoinductive potential. Herein, it can be concluded that the stable, biocompatible and eco-friendly GNPs can be used as an effective bone inductive agent during dental implant therapy.

Biomimetic synthesis of metal–hydroxyapatite (Au-HAp, Ag-HAp, Au-Ag-HAp): Structural analysis, spectroscopic characterization and biomedical application

An innovative biomimetic approach has been employed for the synthesis of human and environmental friendly nanomaterials for biomedical application. The aim of this research is to study the structural analysis of biomimetic-synthesized gold (Au) and silver (Ag) nanoparticles loaded on pristine hydroxyapatite (HAp) and their potential advances in biomedical applications. The synthesized metal–hydroxyapatite nanoparticles’ structural and morphological characteristics were studied using X-ray diffraction (XRD), different spectroscopies (UV–vis, DRS, FTIR, zeta potential), BET surface area and pore size analyzer and electron microscopy (FE-TEM, FE-SEM). Biological activity was established using osteoblast-like MG-63 cell line and antibacterial tests with Escherichia coli (E. coli), which is one of the most common bacteria in the human body. Cell cytotoxicity test (MTT assay and fluorescence imaging with AO/PI staining) was conducted with MG-63 cells to study the toxicity of Au-HAp, Ag-HAp, and Au-Ag-HAp (bimetallic) nanoparticles. Antimicrobial studies have shown that all Ag-HAp nanoparticles have excellent in vitro antibacterial activity with E. coli. The present research investigates the structural stability and biocompatibility of Au-HAp, Ag-HAp, and Au-Ag-HAp nanoparticles, which may be the best materials to repair bone infection (osteomyelitis) and could be useful as a potential scaffold material to prevent postoperative infections.