The majority of the compounds stimulated apoptosis more than 2 times less or concentration. Some agents, such as helenalin perezone, CDDO me, arsenic trioxide, PD 0332991, and amonafide at high concentrations and anthraquinone derivatives topotecan and epoxy at lower concentrations Gamma Secretase cancer were as active on SK N-AS and SH-SY5Y by Lebensf Ability of the test cells, However, caspase 3/7 activity t to a lesser Ausma induced. Profiles contr The inhibition of growth in real time, eight compounds have produced contradictory results concerning the number of cells was evident as blue cell shows reduced, but marginal presence or absence of activated caspase 3/7.
To investigate the cause of these conflicting results, we used the RT that continuously monitor growth patterns of cells for 72 hours after the addition of 30 drugs against NB cell lines with XL147 high and low concentrations. . We found that helenalin perezone, CDDO and causes me to the high concentration of a rapid decline in the number of cells within a few hours after the addition of drugs. Therefore there is probably only a little lebensf Hige cells for the assay of caspase 3/7 in 24 hours after the addition of drugs. Arsenic trioxide, amonafide, and PD 0332991 of high concentration and the EAD and topotecan low in concentration causes a allm Hliche reducing the number of cells, as evidenced by the profiles of the CES RT growth inhibition, and is compatible with a lower degree of induction of caspase 3/7 at 24 hours after the addition of drugs measured.
Cucurbitacin I inhibits the growth of neuroblastoma cells through inhibition of STAT3 we showed that cucurbitacin I was actively have to NB cells and was used as a specific inhibitor of STAT3 described in tumor cells, a number of 10, 11 and this drug can be as a potential be medium to high-risk neuroblastoma. Here we have a further investigation of the inhibition of cell growth and apoptotic activity per t cucurbitacin I with different doses of drugs in a green Eren group of cell lines, including normal MYCN amplified NB cell lines two and three Gheeya et al. Cancer Biol Ther 3 page. Author manuscript, increases available in PMC 27th December 2010. PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript NIH MYCN amplified cell lines do not.
Inhibition of cell growth was detected in all cell lines in a dose-observed Ngigen manner tested, and the induction of apoptosis in a dose of 100 nM or more. We then tested whether the drug also suppresses cell growth through activation of STAT3 in the inhibition of neuroblastoma cells. As shown in Figure 5C, cucurbitacin I reduced H Height of the total STAT3 protein expression in SK AS N, NBEB and SH SY5Y. More importantly, cucurbitacin I also inhibited the phosphorylation of STAT3 in a dose- Ngigen in all four cell lines. These results support saturated That cucurbitacin I cell growth is inhibited by inhibiting the activation of STAT3 NB. Discussion neuroblastoma can not be cured in 60% of patients with advanced disease, 6th In order to find new therapeutic agents for the treatment of NB, we performed a drug screen for compounds with different mechanisms of action of two different cell lines, NB, SK N AS, and SH SY5Y cells, both derived from step 4 tumors 12th These cell lines are repr Sentative MYCN about 75% of patients with NB unverst Markets. NB is a ph Notypisch heterogeneous tumor, displaying neuronal cells, melanocytes or glial / Schwann line 13 These cellular Ren heterogeneity is t both in vitro and, wherever available