Oxidative stress causes bone loss in estrogen-deficient mice through enhanced bone marrow dendritic cell activation

scott submitted, created time 1 year 3 months (www.pnas.org)

Increased production of tumor necrosis factor (TNF) in the bone marrow (BM) in response to both oxidative stress and T cell activation contributes to the bone loss induced by estrogen deficiency, but it is presently unknown whether oxidative stress causes bone loss through T cells.

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Therapeutic effects of STAT3 decoy oligodeoxynucleotide on human lung cancer in xenograft mice

sharkboy submitted, created time 1 year 5 months (www.biomedcentral.com)

"In conclusion, our results suggest that in this model, murine RANKL and not the tumor-derived human RANKL is the mediator of the osteolytic reaction associated with C4-2 growth in bone. They hypothesize that C4-2 cells express other factor/s inducing host production of RANKL, thereby driving tumor-associated osteolysis. "

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UXT is a novel and essential cofactor in the NF-{kappa}B transcriptional enhanceosome

angelfish submitted, created time 1 year 5 months (www.jcb.org)

"As a latent transcription factor, nuclear factor {kappa}B (NF-{kappa}B) translocates from the cytoplasm into the nucleus upon stimulation and mediates the expression of genes that are important in immunity, inflammation, and development. However, little is known about how it is regulated inside the nucleus. By a two-hybrid approach, they identify a prefoldin-like protein, ubiquitously expressed transcript (UXT), that is expressed predominantly and interacts specifically with NF-{kappa}B inside the nucleus

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Repression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) but not its receptors during oral cancer progression

Reviver submitted, created time 1 year 6 months (www.biomedcentral.com)

"Loss of TRAIL expression is an early event during oral carcinogenesis and may be involved in dysregulation of apoptosis and contribute to the molecular carcinogenesis of OSCC. Differential expressions of TRAIL receptors in OSCC do not appear to play a crucial role in their apoptotic rate or metastatic progression."

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