ABT-737 - CAS 852808-04-9
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Not Intended for Therapeutic Use. For research use only.
Bcl-2 Family
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1.ABT-737, a BH3 mimetic, induces glutathione depletion and oxidative stress
Adrienne N. Howard, Kathleen A. Bridges, Raymond E. Meyn, Joya Chandra. Cancer Chemother Pharmacol (2009) 65:41–54
In this study, we used ABT-737 as a tool with which to further test the relationship between Bcl-2 and redox status in a human ALL cell line and in HeLa cells containing a tetracycline (tet)-repressible system for Bcl-2 expression. We find that inhibition of Bcl-2 with ABT-737 lowered intracellular GSH levels, raised intracellular ROS and caused caspase-3-dependent apoptotic DNA fragmentation. Our data suggest a mechanism where inhibition of Bcl-2 by ABT-737 results in a decrease in intracellular GSH, thereby causing caspase activation and apoptosis. We also examined the potential activity of ABT-737 in combination with ROS-inducing chemotherapeutic agents, adaphostin and etoposide, a topoisomerase-II inhibitor, in an effort to apply this knowledge towards devising therapeutic strategies incorporating Bcl-2 inhibition.
2.p53-dependent regulation of Mcl-1 contributes to synergistic cell death by ionizing radiation and the Bcl-2/Bcl-XL inhibitor ABT-737
Katrin E. Tagscherer, Anne Fassl. Apoptosis (2012) 17:187–199
To investigate the effects of a combination treatment with ABT-737 and radiotherapy, we first characterized the glioblastoma cell lines used regarding irradiation response and p53 status. LN229 and U87MG glioblastoma cell lines express wildtype p53, whereas LN18 and U251MG glioblastoma cells express mutant p53. Accordingly, IR-induced the p53 target p21 in LN229 and U87MG cells, but not in LN18 and U251MG cells (Fig. 1a, b). However, regardless of the p53 status IR resulted in a G2/M cell cycle arrest in all cell lines analyzed (Fig. 1c). Next, we investigated the effects of combined IR and ABT-737 treatment on glioblastoma cells. Irradiation followed by treatment with ABT-737 resulted in a synergistic induction of cell death in all cell lines examined (Fig. 1e). This was accompanied by a synergistic cleavage of Caspase 3 (Fig. 1d) suggesting that apoptosis at least partially contributes to the enhancement of cell death, although the involvement of other types of cell death cannot be excluded. Furthermore, we determined whether the chronological order of the single treatments affects the efficacy of the synergistic combination therapy.
3.Methylseleninic acid potentiates multiple types of cancer cells to ABT-737-induced apoptosis by targeting Mcl-1 and Bad
Shutao Yin • Yinhui Dong • Jinghua Li. Apoptosis (2012) 17:388–399
To confirm the role of Akt activation in Bad ser-136 phosphorylation and consequence of Akt activation in apoptosis induction by ABT-737, we tested effects of Akt inactivation by either pharmacological inhibitor or genetic approach on these events in MDA-MB-231 cells. As shown in Fig. 5b (left), under the condition that Akt activation was blocked by its inhibitor LY294002, ABT-737-induced Bad ser-136 phosphorylation was significantly inhibited, whereas ABT-737-induced cleavages of caspases and PARP were dramatically increased. In line with the caspases activation, inhibition of Akt by LY294002 dramatically increased ABT-737-induced apoptosis (Fig. 5b, right). These results were further verified by using siRNA approach. The data are shown in Fig. 5c, ABT-737-induced phosphorylations of Akt and Bad were significantly attenuated by knockdown of Akt, following by significant increase of caspase-3 and PARP cleavages. Taken together, the results strongly suggest that activated Akt confers cancer cells resistant to ABT-737-induced apoptosis which was associated with Bad phosphorylation.
4.Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines
Kimberly A. Foster • Esther P. Jane. J Neurooncol (2014) 120:459–472
Drug resistance remains a major barrier for cancer therapeutics and multiple pathways contribute to cell death resistance in glioma. Studies have shown efficacy of the BH3-mimetic, ABT-737, in hematologic and solid malignancies. We have previously demonstrated that ABT-737 as monotherapy is ineffective in glioma cells and doses of ABT-737 above the clinically achievable range are necessary to suppress cellular proliferation. Several studies have shown that resistance to ABT-737 correlates with levels of Mcl-1 expression. We studied the pharmacologic potential of the adding an HDACI, SAHA, to ABT-737 in malignant glioma. We have previously investigated SAHA in combination therapy in malignant glioma and found induction of apoptosis when used with RTK inhibitors and proteasome inhibitors. The addition of SAHA to ABT-737 reduced cellular proliferation, promoted apoptosis and induced the expression of caspases.
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