Synthesis of Tridax procumbens mediated TiO2 nanoparticles, investigation of antibacterial and anti-cancer activity against selected oral pathogens.

Licochalcone A (Lico-A) is a natural phenol licorice compound with multiple bioactivities, including anti-inflammatory, anti-microbial, anti-fungal and osteogenesis-inducing properties. In the present study, we investigated the Lico-A-induced apoptotic effects and examined the associated apoptosis pathway in KB human oral cancer cells. Lico-A decreased the number of viable KB oral cancer cells. However, Lico-A did not have an effect on primary normal human oral keratinocytes. In addition, the IC50 value of Lico-A was determined to be ~50 μM following dose-dependent stimulation. KB oral cancer cells stimulated with Lico-A for 24 h showed chromatin condensation by DAPI staining, genomic DNA fragmentation by agarose gel electrophoresis and a gradually increased apoptotic cell population by FACS analysis. These data suggest that Lico-A induces apoptosis in KB oral cancer cells. Additionally, Lico-A-induced apoptosis in KB oral cancer cells was mediated by the expression of factor associated suicide ligand (FasL) and activated caspase-8 and −3 and poly(ADP-ribose) polymerase (PARP). Furthermore, in the KB oral cancer cells co-stimulation with a caspase inhibitor (Z-VAD-fmk) and Lico-A significantly abolished the apoptotic phenomena. Our findings demonstrated that Lico-A-induced apoptosis in KB oral cancer cells involves the extrinsic apoptotic signaling pathway, which involves a caspase-dependent FasL-mediated death receptor pathway. Our data suggest that Lico-A be developed as a chemotherapeutic agent for the management of oral cancer.

MicroRNA (miRNA) is a small noncoding RNA molecule, 19-25 nucleotides in length, which regulates several pathways including cell development, cell proliferation, carcinogenesis, apoptosis, etc. In this study, the over-expression of microRNA-205 (miR-205) increased the number of apoptotic cells by at least 4 times compared to the control. In addition, over-expressed miRNA in KB oral cancer cells triggered apoptosis via the caspase cascade, including the cleavage of caspase-9, caspase-7, caspase-3, and PARP. Flow cytometry showed that apoptotic cell death was increased significantly by 35.33% in KB oral cancer cells with over-expressed miR-205 compared to the control. The microarray data showed that axis inhibitor protein 2 (Axin2) was down-regulated in KB oral cancer cells transfected with miR-205. In addition, Axin2 was down-regulated by approximately 50% by over-expressed miR-205 at both the mRNA and protein levels. Interestingly, Axin2 was up-regulated in KB oral cancer compared to human normal oral keratinocytes. Furthermore, the cell cytotoxicity and apoptotic population of KB oral cancer cells were increased significantly after Axin2 siRNA transfection. These results suggest that Axin2 is might be as potential oncogene in KB oral cancer cells. The luciferase assay showed that over-expressed miR-205 in KB oral cancer cells suppressed AXIN2 expression through an interaction with its own binding site at AXIN2 3'UTR (64-92). These results suggest that miR-205 is a novel anti-oncogenic miRNA in KB oral cancer cells, and may have potential applications in oral cancer therapy.

Background Oral squamous cell carcinoma (OSCC) signifies a major global health issue, defined by its destructive nature and often delayed diagnosis, leading to suboptimal prognoses. The global case and mortality rates of OSCC continue to increase, especially among younger populations. Purpose This work aims to study the anti-cancer properties of crebanine on oral cancer KB cells by inducing apoptosis via suppressing PI3K/AKT/mTOR and JAK-2/STAT-3 pathways. Materials and Methods Crebanine at various doses (0.5–25 µM) was evaluated for its in vitro free-radical scavenging properties, including 2,2-diphenyl-1-picrylhydrazyl (DPPH), peroxyl, and superoxide radicals. The impact of crebanine on the growth of oral cancer KB and normal Vero cells was evaluated with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. The mitochondrial membrane potential (MMP) level in untreated and crebanine-treated KB cells was assessed using a fluorescent staining assay. The oxidative stress markers, apoptosis-related proteins, and PI3K/AKT/mTOR and JAK-2/STAT-3 pathway proteins were evaluated in untreated and crebanine-treated KB cells. Results The findings of the free radical scavenging experiments demonstrated the in vitro anti-oxidant properties of crebanine. The findings of the MTT experiment revealed that crebanine considerably inhibited the viability of KB cells without significantly affecting the normal Vero cells. The crebanine treatment reduced the MMP level in KB cells, as demonstrated by the findings of the fluorescent staining assay. The crebanine-treated KB cells exhibited elevated thiobarbituric acid reactive substances (TBARS) levels, alongside decreased glutathione (GSH) and superoxide dismutase (SOD) levels. Furthermore, crebanine treatment enhanced the pro-apoptotic proteins Bax and caspase-3/9 levels, while concurrently inhibiting the PI3K/AKT/mTOR and JAK-2/STAT-3 signaling protein levels in KB cells. Conclusion The current study demonstrates that crebanine treatment can impede cellular proliferation, trigger oxidative stress, and facilitate apoptosis in KB cells via downregulating PI3K/AKT/mTOR and JAK-2/STAT-3 pathways.

Titanium dioxide nanoparticles exhibit good anticancer and antibacterial activities. They are known to be environmentally friendly, stable, less toxic, and have excellent biocompatibility nature. Due to these properties, they are well suited for biological applications particularly in biomedical applications such as drug delivery and cancer therapy. In this research article, three medicinal herbs namely, Plectranthus amboinicus (Karpooravalli), Phyllanthus niruri (Keezhanelli), and Euphorbia hirta (Amman Pacharisi), were used to modify the surface of the TiO2 nanoparticles. The synthesized nanoparticles were subjected to various characterization techniques. The samples are then subjected to MTT assay to determine cell viability. KB oral cancer cells are used for the determination of the anticancer nature of the pure and bio modified nanoparticles. It is observed that Plectranthus amboinicus-Phyllanthus niruri modified TiO2 nanoparticles exhibit excellent anticancer activities among other bio modified and pure samples. The samples are then examined for antibacterial activities against three Gram-negative bacterial strains namely, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and two Gram-positive bacterial strains namely, Staphylococcus aureus and Streptococcus mutans, respectively. Among the modified and pure samples, Plectranthus amboinicus showed good antibacterial activity against Gram-positive and Gram-negative bacteria. In the Flow cytometry analysis, the generation of p53 protein expression from Plectranthus amboinicus-Phyllanthus niruri modified TiO2 nano herbal particles shows the anti-cancerous nature of the sample. Then to determine the toxic nature of the Plectranthus amboinicus-Phyllanthus niruri modified TiO2 nano herbal particles against normal cells, the NPs were subjected to MTT assay against normal L929 cells, and it was found to be safer and less toxic towards the normal cells.

Hydrothermal synthesis of pure and bio modified TiO2: Characterization, evaluation of antibacterial activity against gram positive and gram negative bacteria and anticancer activity against KB Oral cancer cell line

MicroRNA-205 directly regulates the tumor suppressor, interleukin-24, in human KB oral cancer cells.

Green synthesized zinc oxide nanoparticles from Cinnamomum verum bark extract inhibited cell growth and induced caspase-mediated apoptosis in oral cancer KB cells

Background: Oral squamous cell carcinoma (OSCC) is one of the most prevalent and aggressive malignancies, characterized by uncontrolled cell proliferation and high recurrence rates. Despite advancements in therapy, resistance to conventional treatments remains a major challenge. Piperine, a bioactive alkaloid from black pepper, has demonstrated anticancer potential in various cancer models through apoptosis induction and cell cycle arrest. However, its specific effects on oral cancer cell lines remain underexplored. This study evaluates the anticancer activity of Piperine in KB (Human oral cancer) cell line, focusing on its impact on cell viability and apoptotic gene expression. Material and Method: KB oral cancer cells were cultured and treated with Piperine at 25 µM, 50 µM, and 100 µM. Cell viability was assessed using the MTT assay, while morphological changes were observed under an inverted microscope. The expression of key apoptotic genes (Bcl-2, Bax, and p53) was analyzed using quantitative real-time PCR (qRT-PCR). Data were statistically analyzed using one-way ANOVA, and results were expressed as mean ± SEM. Results: Piperine exhibited a dose-dependent cytotoxic effect, significantly reducing cell viability at higher concentrations (50 µM and 100 µM). Microscopic observations revealed cell shrinkage, detachment, and membraneblebbing, indicating apoptotic cell death. Gene expression analysis showed downregulation of Bcl-2 (anti-apoptotic gene) and upregulation of Bax and p53 (pro-apoptotic genes), confirming Piperine induced apoptosis. Conclusion: These findings suggest that Piperine exerts anticancer effects on KB oral cancer cells by inducing apoptosis via the mitochondrial pathway. Its ability to modulate Bcl-2, Bax, and p53 expression highlights its potential as a therapeutic agent for OSCC. Further preclinical and clinical studies are warranted to explore its bioavailability and translational applications in oral cancer therapy.

In the present investigation, green synthesis of silver nanoparticles (AgNPs) was carried out using aqueous leaf extract of Argyreia nervosa. The results of the spectral characterisation have revealed that the surface Plasmon resonance band was observed at 421 nm confirms the formation of AgNPs. The Fourier Transform Infra-red Spectroscopy result shows the reduction of silver nitrate into AgNPs by the reduction of different functional groups. Transmission Electron Microscope analysis revealed that the particles are roughly spherical and poly-disperse in shape and size, the particles are within the size range of 10–55 nm. Dynamic Light Scattering revealed that the nanoparticles were also within the range of 10–50 nm, An-AgNPs have a high negative zeta potential value of −38.9 mV. An-AgNPs showed efficient free radical scavenging activity and showed excellent antimicrobial activity. Anti-proliferative and cytotoxic effect of An-AgNPs was carried out by MTT assay against KB oral cancer cells, the IC50 value of An-AgNPs is 58.64 µg/ml. The cell's growth is arrested at the G2/M phase, so the An-AgNPs activated the Caspase 3 pathway which leads to the Apoptosis of KB oral cancer cells. So it is concluded that the green synthesised An-AgNPs have manifold functions.

The purpose of this study was to examine the effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), an inhibitor of L-type amino acid transporters, on the cell growth suppression in KB human oral cancer cells and to study the roles of cell cycle regulatory factors in the BCH-induced growth inhibition. The effect of BCH on cell growth suppression and the influence of BCH to cell cycle regulatory factors in KB cell growth inhibition were examined using cell cycle analysis, immunoblotting and immunoprecipitation. The BCH treatment induced cell cycle arrest at G1 phase in KB cells. The expression of cyclin D3 was remarkably decreased by BCH treatment. The BCH inhibited the expression of cyclin-dependent protein kinase 6 (CDK6) in a time-dependent manner. In addition, the expression of CDK inhibitor p27 was increased by BCH treatment in KB cells, but not CDK inhibitors p21 and p15. These results suggest that, in KB cells, the inhibition of LAT1 by BCH causes cell cycle arrest at G1 phase by inhibiting cyclin D3-CDK6 complex whereas increasing expression of a CDK inhibitor p27.

Background and Objectives:The perpetual search is on to find botanical complementary adjuncts to the conventional therapies used that is not only cost-effective but also reduces side effects associated with conventional synthetic drugs that are available in the market. The aim of this study was to assess the in vitro anticancer efficacy of hydroalcoholic fruit extract of cranberry against oral cancer KB cell line by Di-Methyl Thiazoldiphenyl Tetrazolium bromide assay (MTT) assay and its cytotoxicity on normal fibroblast cells.Materials and Methods:Vaccinium macrocarpon extract was prepared using a hydroethanolic solvent (water – 30%:ethanol – 70%) using the standardized maceration protocol. Standard KB and normal fibroblast (L929) cell lines were used. The minimum lethal effect of the extract was calculated using the MTT cytotoxicity assay.Results:The extract shows a satisfactory antiproliferative effect on the KB cell line and a higher cell viability percentage of the normal fibroblast cell line.Conclusion:V. macrocarpon can prove to be an adjunct to the existing anticancer drug therapy against oral cancer KB cell line.

Squamous cell carcinoma (SCC) is a malignancy primarily affecting squamous cells. Its development is linked to multiple risk factors, such as alcohol and tobacco consumption, human papillomavirus (HPV) infection, and Epstein-Barr Virus (EBV) infection. Biochanin A (BCA), a phytoestrogen extracted from red clover, has been extensively researched for its therapeutic properties. It spans antioxidant activity, anti-inflammatory effects, neuroprotection, cardioprotection, and anticancer potential in different bodily systems. However, its impact on oral cancer remains unexplored. Therefore, this investigation aims to assess the potential anticancer effects of BCA, specifically on KB oral cancer cells. This study utilized KB cells to evaluate the impact of BCA on various cellular parameters, including cell viability, apoptosis, intracellular ROS production, mitochondrial membrane potential, and cell migration. BCA treatment induced several notable effects on KB cells, including reduced cell viability, altered morphology suggestive of apoptosis, heightened oxidative stress, and alterations in mitochondrial membrane potential. Moreover, BCA treatment demonstrated an inhibitory effect on cell migration. The study further investigated the impact of BCA on antioxidant enzyme activities and lipid peroxidation, revealing decreased antioxidant enzyme activities and increased lipid peroxidation across different BCA concentrations (IC50 and IC90). Immunocytochemistry and qRT-PCR analyses unveiled that BCA treatment at varying doses (IC50 and IC90) downregulated the expression of nuclear factor-κB (NF-κB) subunits p50 and p65, pivotal players in cancer progression. In summary, this study sheds light on the promising potential of BCA as an anticancer therapeutic agent for treating oral cancer. Its demonstrated ability to induce apoptosis, perturb cellular functions, and modulate gene expression within cancer cells underscores its significance. Nonetheless, further research, particularly following animal studies, is imperative to comprehensively grasp the breadth of BCA's effects and its viability for clinical applications.

In the present study, we examined the anticancer properties of berberine in KB oral cancer cells with a specific focus on its cellular mechanism. Berberine did not affect the cell viability of the primary human normal oral keratinocytes that were used as a control. However, the viability of KB cells was found to decrease significantly in the presence of berberine in a dose-dependent manner. Furthermore, in KB cells, berberine induced the fragmentation of genomic DNA, changes in cell morphology, and nuclear condensation. In addition, caspase-3 and -7 activation, and an increase in apoptosis were observed. Berberine was also found to upregulate significantly the expression of the death receptor ligand, FasL. In turn, this upregulation triggered the activation of pro-apoptotic factors such as caspase-8, -9 and -3 and poly(ADP-ribose) polymerase (PARP). Furthermore, pro-apoptotic factors such as Bax, Bad and Apaf-1 were also significantly upregulated by berberine. Anti-apoptotic factors such as Bcl-2 and Bcl-xL were downregulated. Z-VAD-FMK, a cell-permeable pan-caspase inhibitor, suppressed the activation of caspase-3 and PARP. These results clearly indicate that berberine-induced cell death of KB oral cancer cells was mediated by both extrinsic death receptor-dependent and intrinsic mitochondrial-dependent apoptotic signaling pathways. In addition, berberine-induced upregulation of FasL was shown to be mediated by the p38 MAPK signaling pathway. We also found that berberine-induced migration suppression was mediated by downregulation of MMP-2 and MMP-9 through phosphorylation of p38 MAPK. In summary, berberine has the potential to be used as a chemotherapeutic agent, with limited side-effects, for the management of oral cancer.

Bio-modified TiO2 nanoparticles with Withania somnifera, Eclipta prostrata and Glycyrrhiza glabra for anticancer and antibacterial applications.

Introduction Citrus fruit peels contain Tangeretin, a natural chemical flavonoid that reinforces plant cell walls and serves as a defense mechanism. Apoptosis, growth inhibition, anti-oxidant, anti-diabetic, and anti-cancer activities are only a few of its many qualities. Tangeretin's principal function is to shield healthy cells or tissues from the harmful effects of chemotherapy. The purpose of this study was to investigate the apoptotic activity of Tangeretin's impact on KB (oral cancer cells) cell lines. Materials and method This study employed Tangeritin, in investigating its effects on oral cancer cells. Oral cancer cells were cultured in Dulbecco's modified Eagle's medium (DMEM), with 10% fetal bovine serum at 37°C in a 5% CO2 environment. Cell viability was assessed by seeding oral cancer cells in 96-well plates, exposing them to varying Tangeritin concentrations (50 µM, 100 µM, and 200 µM) with growth inhibition of KB cell viability in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assayand morphological changes in cells were observed under an inverted light microscope at 10x magnification. The results were reported as mean±standard error mean (SEM) using one-way analysis of variancethrough IBM SPSS Statistics for Windows, Version 23 (Released 2015; IBM Corp., Armonk, New York, United States). Result MTT assay showed a significant reduction in KB cell viability when treated with Tangeretin. With asignificant decrease in mRNA levels of the anti-apoptotic genes Bcl-2 and Bcl-xL. At 50 µM, 100 µM, and 200 µM, the levels of Bcl-2 were 0.85 ± 0.09, 0.62 ± 0.05, and 0.67 ± 0.05, respectively. Similarly, the mRNA expression of Bcl-xL was 0.82 ± 0.07 for 50 µM, 0.7 ± 0.06 for 100 µM, and 0.77 ± 0.06for 200 µM. The mRNA expression levels of Bax were 1.1 ± 0.09 for 50 µM, 1.4 ± 0.12for 100 µM, and 1.3 ± 0.11 for 200 µM, respectively. Conclusion Tangeretin showed a promising apoptotic activity in KB cells suggesting its utility as an anti-cancer compound. It prevented the growth and proliferation of cancer cells by acting on pro-apoptotic and anti-apoptotic genes. However, this conclusion is mostly based on the in vitro study. Therefore in vivo animal studies were needed to confirm the findings.