Using a simple method of mass production of green carbon nanotags (G-tags) from harmful cyanobacteria, we developed an advanced and efficient imaging platform for the purpose of anticancer therapy. Approximately 100 grams of G-tags per 100 kilograms of harmful cyanobacteria were prepared using our eco-friendly approach. The G-tags possess high solubility, excellent photostability, and low cytotoxicity (<1.5 mg/mL for 24 h). Moreover, doxorubicin-conjugated G-tags (T-tags; >0.1 mg/mL) induced death in cancer cells (HepG2 and MCF-7) in-vitro at a higher rate than that of only G-tags while in-vivo mice experiment showed enhanced anticancer efficacy by T-tags at 0.01 mg/mL, indicating that the loaded doxorubicin retains its pharmaceutical activity. The cancer cell uptake and intracellular location of the G- and T-tags were observed. The results indicate that these multifunctional T-tags can deliver doxorubicin to the targeted cancer cells and sense the delivery of doxorubicin by activating the fluorescence of G-tags.

The posttranslational modification of neural cell-adhesion molecule (NCAM) with polysialic acid (PSA) and the spatiotemporal distribution of PSA-NCAM play an important role in the neuronal development. In this work, we developed a tissue-based strategy for metabolically incorporating an unnatural monosaccharide, peracetylated N-azidoacetyl-D-mannosamine, in the sialic acid biochemical pathway to present N-azidoacetyl sialic acid to PSA-NCAM. Although significant neurotoxicity was observed in the conventional metabolic labeling that used the dissociated neuron cells, neurotoxicity disappeared in this modified strategy, allowing for investigation of the temporal and spatial distributions of PSA in the primary hippocampal neurons. PSA-NCAM was synthesized and recycled continuously during neuronal development, and the two-color labeling showed that newly synthesized PSANCAMs were transported and inserted mainly to the growing neurites and not significantly to the cell body. This report suggests a reliable and cytocompatible method for in vitro analysis of glycans complementary to the conventional cell-based metabolic labeling for chemical glycobiology.

Telomerase activation is a key step in the development of human cancers. Interferon-β (IFN-β) signaling induces growth arrest in many tumors but the anticancer mechanism of IFN-β is poorly understood. In the present study, we show that IFN-β signaling represses telomerase activity and human telomerase reverse transcriptase (hTERT) transcription in ovarian cancer and suggest that this signaling is mediated by p21(WAF1). IFN-β triggered down-regulation of telomerase activity and hTERT mRNA expression and also induced p21 expression, independently of p53 induction. Ectopic expression of p21 attenuated hTERT promoter activity. Murine embryonic fibroblasts (MEFs) genetically deficient in p21 (p21-/-) showed elevated (> 15 times) hTERT promoter activity compared to wild-type MEFs. Overexpression of p21 reduced the hTERT promoter activity of p21-/- MEFs and hTERT mRNA expression in HCT119 p21(WAF1) null cell. These findings provide evidence that p21 is a potential mediator of IFN-β-induced attenuation of telomerase activity and tumor suppression.

Objectives:Modified regular ginseng extract (MRGX) has stronger anti-cancer activity-possessing gensenoside profiles.Methods:To investigate changes in gene expression in the MRGX-treated lung cancer cells (A549), we examined genomic data with cDNA microarray results. After completing the gene-ontology-based analysis, we grouped the genes into up-and down-regulated profiles and into ontology-related regulated genes and proteins through their interaction network.Results:One hundred nine proteins that were up- and down-regulated by MRGX were queried by using IPA. IL8, MMP7 and PLAUR and were found to play a major role in the anti-cancer activity in MRGX-treated lung cancer cells. These results were validated using a Western blot analysis and a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis.Conclusions:Most MRGX-responsive genes are up-regulated transiently in A549 cells, but down-regulated in a sustained manner in lung cancer cells.