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 Post subject: Fetal bovine serum is normally added to the culture medium,
PostPosted: Wed Mar 26, 2014 11:34 pm 
Saab Warrior

Joined: Tue Mar 18, 2014 1:05 am
Posts: 66
One potential explanation might be that endogenous cytoplasmic Sirt1 levels in comparison to nuclear ex pression levels are too low to be detected by our anti body. Another explanation would be that cytoplasmic Sirt1 plays a major role in the development of purchase KU-0063794 carcino genic precursors and nuclear Sirt1 has its place in the fully developed cancer. However, this has to be inves tigated in future functional studies. Interestingly, following up the seminal work by Luo et al. and Vasiri et al. a very recent study by Li and co workers explored the Sirt1 p53 axis in chronic mye loid leukemia and found that targeting of Sirt1 by either shRNA or the small molecule inhibitor tenovin 6 resulted in increased levels of acetylated p53 in CML CD34 cells accompanied by increased transcriptional ac tivity of p53.<br><br> Abrogation of Sirt1 led to growth inhibition and reduced engraftment of the tumor cells. These effects were even more pronounced when cells were synergistic ally treated with the tyrosine kinase inhibitor imatinib. These data purchase Lenalidomide strengthen the view of a context dependent tumorigenic impact of Sirt1 as also suggested by our re sults. Since p53 aberrations are commonly involved in PDAC tumorigenesis, it is tempting to speculate whether Sirt1 inhibition may help to restore the remaining functionally intact p53 pool. Indeed, recent data indi cate that downregulation of Sirt1 by restoration of HIC1 leads to increased levels of acetylated p53 and upregulated p21 in pancreatic cancer. On cellular level, overexpressed HIC1, which in turn led to downregulation Sirt1 resulted in cell cycle arrest and apop tosis.<br><br> Loss of p53 function has also been implicated in re sistance to EGFR targeting strategies, the latter having a limited but significant role in the treatment of PDACs. Interestingly, we observed a synergistic impact of combined Sirt1 and EGFR inhibition suggesting a func tional interdependence in PDACs, whose molecular details remain to be explored. In prostatic LY2603618 ic50 cancer cells Byles and colleagues observed Sirt1 to modulate EMT upon EGF signalling via the induction of the transcription factor ZEB1. Although it remains to be investigated whether this mechanism works in PDACs, our data and these results may additionally point to a therapeutic rationale for com bined EGFRSirt1 inhibition.<br><br> While a number of small molecule inhibitors of class I and II HDACs are currently in clinical trials for the treatment of malignancies of various organ origins, SIRT1 inhibition is currently only investigated in a phase I trial of patients with Huntingtons disease. Conclusions In conclusion, there is accumulating evidence that Sirt1 has an oncogenic role in PDACs and provided that further studies are able to reproduce and extent the data presented herein towards mouse model systems, a clinical trial for pa tients with PDAC, whose outcome and treatment options are extremely limited for the vast majority of patients, may be worthwhile to consider. Background Thyroid cancer is the most common malignant tumor in endocrine system, and its incidence has been steadily in creasing in many regions of the world. Follicular epithelial cell derived thyroid tumors are the most com mon type, accounting for about 95 97% of all thyroid malignancies, and are histologically classified into fol licular adenoma, papillary thyroid cancer, follicular thyroid cancer, and anaplastic thyroid cancer.

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