Home LiteratureArticle Details
PMID: 11576999 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

p53-independent apoptosis mediated by tachpyridine, an anti-cancer iron chelator.

Carcinogenesis ·Vol. 22 ·No. 10 ·2001-10-00 ·Pages 1607-14

Abeysinghe RD, Greene BT, Haynes R, Willingham MC, Turner J, Planalp RP, Brechbiel MW, Torti FM, Torti SV

Abstract

Iron is involved in essential biochemical reactions ranging from respiration to DNA synthesis. Consequently, iron deprivation has been proposed as a strategy for inhibition of tumor cell growth. We recently described a novel iron chelator, tachypyridine [N,N',N"-tris(2-pyridylmethyl)-cis,cis-1,3,5-triaminocyclohexane], and demonstrated that it not only inhibited growth of cultured tumor cells, but was actively cytotoxic. Here we explore the mechanisms underlying tachpyridine cytotoxicity. Using several criteria, including time-lapse video microscopy, DNA staining and TUNEL assays, tachpyridine was shown to specifically induce apoptotic cell death. Further, unlike numerous cytotoxic chemotherapeutic drugs which induce apoptosis by activating p53-dependent pathways, tachpyridine-mediated cell death did not require p53 activation. Although immunoblotting revealed rapid accumulation of p53 following treatment with tachpyridine, p21(WAF1) was not induced. Further, neither cytotoxicity nor apoptosis required p53. p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system. Further, time-lapse video microscopy and TUNEL assays demonstrated that both p53 null and p53 wild-type cells underwent apoptotic cell death in response to tachpyridine. In addition, in 55 human cancer cell lines the mean GI(50) of tachpyridine in cells with mutant p53 was virtually identical to the GI(50) in cells with wild-type p53. These results demonstrate that tachpyridine initiates an apoptotic mode of cell death that does not require functional p53. Since over 50% of human tumors contain a functionally defective p53 that reduces sensitivity to commonly used chemotherapeutic agents, such as etoposide and cisplatin, the ability of tachpyridine to induce apoptosis independently of p53 may offer an advantage in anti-tumor therapy.

MeSH Terms
Anticarcinogenic Agents/pharmacology Apoptosis/drug effects Cell Cycle/drug effects Cell Division/drug effects Colony-Forming Units Assay Cyclin-Dependent Kinase Inhibitor p21 Cyclins/metabolism Cyclohexylamines/pharmacology DNA, Neoplasm/drug effects Drug Screening Assays, Antitumor Humans In Situ Nick-End Labeling Iron Chelating Agents/pharmacology Mutation Pyridines/pharmacology Transfection Tumor Cells, Cultured/drug effects,metabolism Tumor Suppressor Protein p53/metabolism
Chemicals
Anticarcinogenic Agents CDKN1A protein, human Cyclin-Dependent Kinase Inhibitor p21 Cyclins Cyclohexylamines DNA, Neoplasm Iron Chelating Agents Pyridines Tumor Suppressor Protein p53 tachpyr
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Abeysinghe R D
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Greene B T
Haynes R
Willingham M C
Turner J
Planalp R P
Brechbiel M W
Torti F M
Torti S V
Article Info
Journal
Carcinogenesis
Abbr.
Carcinogenesis
ISSN
0143-3334
Published
2001-10-00
Pages
1607-14
Language
English
Region
England
NLM ID
8008055
Subset
IM
Grants
NIDDK NIH HHS · DK 57781 · United States
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]