Home LiteratureArticle Details
PMID: 1873814 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Programmed death of nonproliferating androgen-independent prostatic cancer cells.

Cancer research ·Vol. 51 ·No. 17 ·1991-09-01 ·Pages 4693-700

Martikainen P, Kyprianou N, Tucker RW, Isaacs JT

Abstract

Androgen ablation induces an energy-dependent process of programmed death in nonproliferating androgen-dependent prostatic cancer cells which involves fragmentation of genomic DNA into nucleosomal oligomers catalyzed by nuclear Ca2+, Mg(2+)-dependent endonuclease enzymes activated following a sustained elevation in intracellular free Ca2+ (Cai). In contrast, androgen-independent prostatic cancer cells are not induced to undergo such programmed cell death by androgen ablation. One explanation for the inability of androgen ablation to induce programmed death of androgen-independent prostatic cancer cells is that such ablation does not result in a sustained elevation in Cai in these cells. This raises the issue of whether androgen-independent prostatic cancer cells can be induced to undergo programmed death if an elevation in the Cai is sufficiently sustained by nonhormonal means. To test this possibility, androgen-independent, highly metastatic Dunning R-3327 AT-3 rat prostatic cancer cells were chronically exposed in vitro to the calcium ionophore ionomycin to sustain an elevation in their Cai. These studies demonstrated that an elevation of Cai as small as only 3-6-fold above baseline can induce the death of these cells if sustained for greater than 12 h. Temporal analysis demonstrated that the death of these cells does not require cell proliferation and involves Ca(2+)-induced fragmentation of genomic DNA into nucleosome-sized pieces as the commitment step in this process. These results demonstrate that even nonproliferating androgen-independent prostatic cancer cells can be induced to undergo programmed cell death if a modest elevation in the Cai is sustained for a sufficient time. These observations identify Cai as a potential target for therapy for androgen-independent prostatic cancer cells.

MeSH Terms
Calcium/metabolism Cell Cycle/drug effects Cell Division Cell Survival DNA Damage DNA, Neoplasm/drug effects Gene Expression Regulation, Neoplastic/genetics Humans Ionomycin/pharmacology Male Microscopy, Electron Microscopy, Electron, Scanning Prostatic Neoplasms/genetics,metabolism,pathology,ultrastructure RNA, Messenger/analysis RNA, Neoplasm/analysis Time Factors
Chemicals
DNA, Neoplasm RNA, Messenger RNA, Neoplasm Ionomycin Calcium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Martikainen P
Johns Hopkins Oncology Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21205.
Kyprianou N
Tucker R W
Isaacs J T
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
1991-09-01
Pages
4693-700
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
Grants
NCI NIH HHS · 5-P30-CA06973 · United States
NCI NIH HHS · CA50601 · United States
OHS HRSA HHS · FOSTW04050 · 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: product@genelibs.com