Morphological evolution of upconversion nanoparticles and their biomedical signal generation.

Advancements in the fabrication of upconversion nanoparticles (UCNPs) for synthetic control can enable a broad range of applications in biomedical systems. Herein, we experimentally verified the role of the hydrothermal reaction (HR) time in the synthesis of NaYF4:20%Yb3+/3%Er3+ UCNPs on their morphological evolution and phase transformation at different temperatures. Characterizations of the as-prepared UCNPs were conducted using X-ray diffraction (XRD), electron microscopy and spectroscopy, and thermogravimetric and upconversion (UC) luminescence analysis. We demonstrated that determining the optimal HR time, also referred to here as the threshold time, can produce particles with good homogeneity, hexagonal phase, and UC luminescence efficiency. Subsequently, the polymer coated UCNPs maintained their original particle size distribution and luminescence properties, and showed improved dispersibility in a variety of solvents, cellular nontoxicity, in vitro bioimaging, and biocompatibility as compared to the bare UCNP. Besides this, polyacrylic acid conjugated UCNPs (UCNP@PAA) also revealed the strong anticancer effect by conjugating with doxorubicin (DOX) as compared to the free DOX. Based on these findings, we suggest that these particles will be useful in drug-delivery systems and as in vivo bioimaging agents synchronously.

Induction of p73beta by a naphthoquinone analog is mediated by E2F-1 and triggers apoptosis in HeLa cells.

Recently, p73 was identified as a structural and functional homolog of p53. The p73 protein activates the transcription of genes downstream of p53 and induces apoptosis when overexpressed in several cell lines, similar to the tumor suppressor p53. However, the extracellular stimuli and molecular mechanisms regulating p73 activity remain to be elucidated. In this paper, we present evidence that the naphthoquinone analog, 2,3-dichloro-5,8-dihydroxy-1,4-naphthoquinone (NA), is a novel apoptotic stimulus that induces p73beta expression. Treatment with NA induced the expression of p73beta mRNA and protein and its downstream genes, p21 and bax, in HeLa cells. Similar results were obtained in MCF7 cells (p53(+/+), p73(+/+)). In the MCF7 cells, p53 protein level was rather decreased by NA treatment. Overexpression of p73beta led to the apoptosis of HeLa cells and enhancement of NA-induced cell death. Expression of p73beta was mediated by E2F-1, which was activated via release from pRB after exposure of cells to NA. We additionally observed that overexpression of pRB inhibited NA-induced apoptosis. These results imply that p53-independent p73beta-dependent p21 expression is involved in NA-induced apoptosis of HeLa cells.