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Engineered nanoparticles are increasingly being considered for use as biosensors, imaging agents and drug delivery vehicles. Their versatility in design and applications make them an attractive proposition for new biological and biomedical approaches. Despite the remarkable speed of development in nanoscience, relatively little is known about the interaction of nanoscale objects with living systems. In a biological fluid, proteins associate with nanoparticles, and the amount and the presentation of the proteins on their surface could lead to a different in vivo response than an uncoated particle. Here, in addition to protein adsorption, we are going to introduce concept of cell "vision", which would be recognized as another crucial factor that should be considered for the safe design of any type of nanoparticles that will be used in specific biomedical applications. The impact of exactly the same nanoparticles on various cells is significantly different and could not be assumed for other cells; the possible mechanisms that justify this cellular response relate to the numerous detoxification strategies that any particular cell can utilize in response to nanoparticles. The uptake and defence mechanism could be considerably different according to the cell type. Thus, what the cell "sees", when it is faced with nanoparticles, is most likely dependent on the cell type.

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Overexpression of DNA methyltransferase 1 (DNMT-1) is observed mostly in pancreatic cancer and it can cause tumor suppressor genes silencing in this disease. Recent studies suggest that abnormal expressions of microRNAs (miRs) are involved in pathogenesis of different types of human cancers including pancreatic cancer. In this study we aimed to investigate the effect of miR-148b and -152 on reverting the tumorigenic phenotype of pancreatic cancer cell lines. In order to investigate whether miR-148b and -152 are involved in the regulation of DNMT-1, luciferase reporter assay was used and confirmed that the DNMT-1 mRNA could be a target for miR-148b and miR-152. Furthermore, overexpression of miR-148b and -152 in pancreatic cancer cell lines (MIA PaCa-2 and AsPC-1) decreased DNMT-1 expression (53% and 59% respectively), returned DNA methylation to normal patterns and induced re-expression of tumor suppressor genes, like BNIP3 (4.7- and 3.8-fold) and SPARC (5.3- and 2.9-fold) for miR-148b and -152 respectively. Moreover, the introduced miR-148b and -152 could inhibit the proliferation of MIA PaCa-2 (35% and 37% respectively) and AsPC-1 (39% and 40% respectively) cell lines. The apoptosis rates of MIA PaCa-1 after treatment with miR-148b and -152 were 10% and 8% respectively; while these rates in AsPC-1 were 16% and 11% respectively. Conclusively these findings mean that miRs that are targeting DNMT-1 and modifying methylation status of tumor suppressor genes such as BNIP3 and SPARC can be applied in killing the pancreatic cancer cells and decreasing the tumorigenicity of these cells.