Carboxyl nanodiamonds inhibit melanoma tumor metastases by blocking cellular motility and invasiveness.

Carboxyl nanodiamond (cND) nanoparticles are actively internalized by B16F10 melanoma cells in culture. Treatment of B16F10 tumor cells with cNDs in vitro inhibited their ability to (i) migrate and invade through porous membranes in a transwell culture system, (ii) secrete matrix metalloproteinases (MMPs) MMP-2 and MMP-9, and (iii) express selected epithelial-mesenchymal transition markers critical for cell migration and invasion. Administration of luciferase-transfected B16F10-Luc2 melanoma cells resulted in a rapid growth of the tumor and its metastasis to different organs that could be monitored by in vivo bioluminescence imaging as well as by ex vivo BLI of the mouse organs. After tumor cells were administered intravenously in C57Bl/6 mice, administration of cNDs (50 µg i.v. every alternate day) resulted in marked suppression of the tumor growth and metastasis in different organs of mice. Subcutaneous administration of B16F10 cells resulted in robust growth of the primary tumor subcutaneously as well as its metastasis to the lungs, liver, spleen, and kidneys. Intravenous treatment with cNDs did not affect the growth of the primary tumor mass but essentially blocked the metastasis of the tumor to different organs. Histological examination of mouse organs indicated that the administration of cNDs by itself was safe and did not cause toxic changes in mouse organs. These results indicate that the cND treatment may have an antimetastatic effect on the spread of B16F10 melanoma tumor cells in mice. Further exploration of cNDs as a possible antimetastatic therapeutic agent is suggested.

Cost-effective synthesis of 2D molybdenum disulfide (MoS2) nanocrystals: An exploration of the influence on cellular uptake, cytotoxicity, and bio-imaging.

Ultrasmall MoS2 nanocrystals have unique optoelectronic and catalytic properties that have acquired significant attraction in many areas. We propose here a simple and economical method for synthesizing the luminescent nanocrystals MoS2 using the hydrothermal technique. In addition, the synthesized MoS2 nanocrystals display photoluminescence that is tunable according to size. MoS2 nanocrystals have many advantages, such as stable dispersion, low toxicity and luminescent characteristics, offering their encouraging applicability in biomedical disciplines. In this study, human lung cancer epithelial cells (A549) are used to assess fluorescence imaging of MoS2 nanocrystals. MTT assay, trypan blue assay, flow cytometry and fluorescence imaging results have shown that MoS2 nanocrystals can selectively target and destroy lung cancer cells, especially drug-resistant cells (A549).

Nanodiamonds inhibit scratch-wound repair in lung epithelial cell monolayers by blocking cell migration and inhibiting cell proliferation.

Proliferation and migration of lung epithelial cells following the injury to the epithelial lining of alveoli and airways in the lung are pivotal for remodeling and repair of the wound to restore normal lung function. In the present study, we examined the modulatory effect of carboxylated nanodiamonds (cNDs) on the cell division, migration, and adhesion of epithelial cells in the well-established in vitro model of wound repair and cell migration. Flow cytometry and confocal microscopy results indicated that both LA4 and A549 cells effectively internalized fluorescent carboxylated nanodiamonds (cFNDs) and the internalized nanodiamonds were essentially localized in the cytoplasmic region. Treatment with cNDs blocked the division and migration of cells to fill the scratch wound. Live cell imaging and time-lapse videography of the wound healing process indicated a significant inhibition of cell proliferation activity in cND-treated cells and blocked the wound repair process. Trans-well cell-migration assay results further support the inhibitory effect of cNDs on the cell migration process. Western blotting and immunofluorescence staining indicated that the crucial proteins involved in epithelial-mesenchymal transition (EMT) and cell migration i.e. ß-catenin, Vimentin, NM-myosin, and Focal Adhesion Kinase (FAK) were downregulated after treatment with cNDs, while the expression of E-cadherin and Claudin-1, major cell adhesion markers remained unaltered. Taken together, our results indicate that the decline in cell proliferation activity, downregulation in the expression of various crucial protein like ß-Catenin, NM-myosin, FAK, and Vimentin involved in the cell migration and unaltered expression of cell adhesion molecules E-cadherin and Claudin-1, may be the factors that contribute to the cND-mediated inhibition of EMT during the wound repair process in the monolayers of lung epithelial cells.