Activation of the c-Jun N-terminal Kinase/Activating Transcription Factor 3 (ATF3) Pathway Characterizes Effective Arylated Diazeniumdiolate-Based Nitric Oxide-Releasing Anticancer Prodrugs-Reference-Cited by-同舟云学术

Activation of the c-Jun N-terminal Kinase/Activating Transcription Factor 3 (ATF3) Pathway Characterizes Effective Arylated Diazeniumdiolate-Based Nitric Oxide-Releasing Anticancer Prodrugs

Published:2011-10-28 Issue:22 Volume:54 Page:7751-7758
ISSN:0022-2623
Container-title:Journal of Medicinal Chemistry
language:en
Short-container-title:J. Med. Chem.

Author:

Maciag Anna E.¹,Nandurdikar Rahul S.²,Hong Sam Y.²,Chakrapani Harinath³,Diwan Bhalchandra¹,Morris Nicole L.⁴,Shami Paul J.⁵,Shiao Yih-Horng²,Anderson Lucy M.²,Keefer Larry K.²,Saavedra Joseph E.¹

Affiliation:

1. Basic Science Program, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland 21702, United States

2. Chemical Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702, United States

3. Department of Chemistry, Indian Institute of Science Education and Research, Pune 411008, India

4. Laboratory Animal Sciences Program, SAIC-Frederick, Inc., National Cancer Institute, Frederick, Maryland 21702, United States

5. Division of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, United States

Publisher

American Chemical Society (ACS)

Subject

Drug Discovery,Molecular Medicine

Link

https://pubs.acs.org/doi/pdf/10.1021/jm2004128

Reference22 articles.

1. Comparison of Four Chemotherapy Regimens for Advanced Non–Small-Cell Lung Cancer

2. Antitumor Activity of JS-K [O2-(2,4-Dinitrophenyl) 1-[(4-Ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate] and Related O2-Aryl Diazeniumdiolates in Vitro and in Vivo

3. JS-K, a novel non-ionic diazeniumdiolate derivative, inhibits Hep 3B hepatoma cell growth and induces c-Jun phosphorylation via multiple MAP kinase pathways

4. JS-K, a GST-activated nitric oxide generator, induces DNA double-strand breaks, activates DNA damage response pathways, and induces apoptosis in vitro and in vivo in human multiple myeloma cells

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