Literature DB >> 17085670

Schedule-dependent synergy between the heat shock protein 90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin and doxorubicin restores apoptosis to p53-mutant lymphoma cell lines.

Ana I Robles1, Mollie H Wright, Bheru Gandhi, Steven S Feis, Christin L Hanigan, Adrian Wiestner, Lyuba Varticovski.   

Abstract

PURPOSE: Loss of p53 function impairs apoptosis induced by DNA-damaging agents used for cancer therapy. Here, we examined the effect of the heat shock protein 90 (HSP90) inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin (DMAG) on doxorubicin-induced apoptosis in lymphoma. We aimed to establish the optimal schedule for administration of both drugs in combination and the molecular basis for their interaction. EXPERIMENTAL
DESIGN: Isogenic lymphoblastoid and nonisogenic lymphoma cell lines differing in p53 status were exposed to each drug or combination. Drug effects were examined using Annexin V, active caspase-3, cell cycle, and cytotoxicity assays. Synergy was evaluated by median effect/combination index. Protein expression and kinase inhibition provided insight into the molecular mechanisms of drug interaction.
RESULTS: Presence of mutant p53 conferred increased survival to single agents. Nevertheless, DMAG showed synergistic toxicity with doxorubicin independently of p53 status. Synergy required exposure to doxorubicin before DMAG. DMAG-mediated down-regulation of CHK1, a known HSP90 client, forced doxorubicin-treated cells into premature mitosis followed by apoptosis. A CHK1 inhibitor, SB-218078, reproduced the effect of DMAG. Administration of DMAG before doxorubicin resulted in G1-S arrest and protection from apoptosis, leading to additive or antagonistic interactions that were exacerbated by p53 mutation.
CONCLUSIONS: Administration of DMAG to doxorubicin-primed cells induced premature mitosis and had a synergistic effect on apoptosis regardless of p53 status. These observations provide a rationale for prospective clinical trials and stress the need to consider schedule of exposure as a critical determinant of the overall response when DMAG is combined with chemotherapeutic agents for the treatment of patients with relapsed/refractory disease.

Entities:  

Mesh:

Substances:

Year:  2006        PMID: 17085670     DOI: 10.1158/1078-0432.CCR-06-1178

Source DB:  PubMed          Journal:  Clin Cancer Res        ISSN: 1078-0432            Impact factor:   12.531


  18 in total

1.  Hsp90 inhibitors block outgrowth of EBV-infected malignant cells in vitro and in vivo through an EBNA1-dependent mechanism.

Authors:  Xiaoping Sun; Elizabeth A Barlow; Shidong Ma; Stacy R Hagemeier; Sarah J Duellman; Richard R Burgess; Judy Tellam; Rajiv Khanna; Shannon C Kenney
Journal:  Proc Natl Acad Sci U S A       Date:  2010-01-26       Impact factor: 11.205

2.  Schedule-dependent synergy of histone deacetylase inhibitors with DNA damaging agents in small cell lung cancer.

Authors:  Victoria L Luchenko; Crystal D Salcido; Yongwei Zhang; Keli Agama; Edina Komlodi-Pasztor; Robert F Murphy; Giuseppe Giaccone; Yves Pommier; Susan E Bates; Lyuba Varticovski
Journal:  Cell Cycle       Date:  2011-09-15       Impact factor: 4.534

3.  Novel HSP90 inhibitors, NVP-AUY922 and NVP-BEP800, radiosensitise tumour cells through cell-cycle impairment, increased DNA damage and repair protraction.

Authors:  L Stingl; T Stühmer; M Chatterjee; M R Jensen; M Flentje; C S Djuzenova
Journal:  Br J Cancer       Date:  2010-05-25       Impact factor: 7.640

4.  Heat shock protein 90 inhibitors: new mode of therapy to overcome endocrine resistance.

Authors:  Cynthie Wong; Shiuan Chen
Journal:  Cancer Res       Date:  2009-10-27       Impact factor: 12.701

Review 5.  Heat shock proteins in animal neoplasms and human tumours--a comparison.

Authors:  Mariarita Romanucci; Tania Bastow; Leonardo Della Salda
Journal:  Cell Stress Chaperones       Date:  2008-03-12       Impact factor: 3.667

6.  Geldanamycin promotes premature mitotic entry and micronucleation in irradiated p53/p21 deficient colon carcinoma cells.

Authors:  D M Moran; G Gawlak; M S Jayaprakash; S Mayar; C G Maki
Journal:  Oncogene       Date:  2008-05-26       Impact factor: 9.867

Review 7.  ATR/CHK1 inhibitors and cancer therapy.

Authors:  Zhaojun Qiu; Nancy L Oleinick; Junran Zhang
Journal:  Radiother Oncol       Date:  2017-10-18       Impact factor: 6.280

8.  HSP90 inhibitor, DMAG, synergizes with radiation of lung cancer cells by interfering with base excision and ATM-mediated DNA repair.

Authors:  Thuy T Koll; Steven S Feis; Mollie H Wright; Modupe M Teniola; Mekel M Richardson; Ana I Robles; John Bradsher; Jacek Capala; Lyuba Varticovski
Journal:  Mol Cancer Ther       Date:  2008-07       Impact factor: 6.261

9.  Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence.

Authors:  Kaori Fujita; Izumi Horikawa; Abdul M Mondal; Lisa M Miller Jenkins; Ettore Appella; Borivoj Vojtesek; Jean-Christophe Bourdon; David P Lane; Curtis C Harris
Journal:  Nat Cell Biol       Date:  2010-11-07       Impact factor: 28.824

10.  A purine scaffold Hsp90 inhibitor destabilizes BCL-6 and has specific antitumor activity in BCL-6-dependent B cell lymphomas.

Authors:  Leandro C Cerchietti; Eloisi C Lopes; Shao Ning Yang; Katerina Hatzi; Karen L Bunting; Lucas A Tsikitas; Alka Mallik; Ana I Robles; Jennifer Walling; Lyuba Varticovski; Rita Shaknovich; Kapil N Bhalla; Gabriela Chiosis; Ari Melnick
Journal:  Nat Med       Date:  2009-11-22       Impact factor: 53.440

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.