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Glucocorticoids augment survival and proliferation of tumor cells.
Anticancer Res. 32, 4251-4261 (2012)
BACKGROUND: Glucocorticoids are widely used for cancer patients, although they can reduce the efficacy of anticancer treatment. MATERIALS AND METHODS: We characterized non-apoptotic actions of glucocorticoids on tumor cell lines, primary tumor cells and an in vivo model, together with molecular signaling studies. RESULTS: Glucocorticoids enhanced cell proliferation in 9/17 cell lines and significantly promoted tumor cell proliferation in a pre-clinical mouse model of lung carcinoma. 65/139 primary acute childhood leukemia samples were glucocorticoid-resistant. Both dexamethasone and prednisolone increased in vitro survival in 21/65 samples from glucocorticoid-resistant primary leukemias, revealing a completely new action of glucocorticoids. Dexamethasone-induced proliferation was mediated by glucocorticoid receptor and activated the proliferation signaling pathways of protein kinase B/AKT and p38 mitogen-activated protein kinase. CONCLUSION: Our data suggest that restriction of the use of glucocorticoids during anticancer treatment might improve the outcome of patients with solid tumors.
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1.725
0.658
40
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Tumor cell proliferation; glucocorticoids; glucocorticoid receptor; p38MAPK; AKT; ACUTE LYMPHOBLASTIC-LEUKEMIA; INDUCED APOPTOSIS; BRAIN METASTASES; LUNG-CANCER; DEXAMETHASONE; RECEPTOR; PHARMACOKINETICS; PREDNISOLONE; STIMULATION; PACLITAXEL
Language
english
Publication Year
2012
HGF-reported in Year
2012
ISSN (print) / ISBN
0250-7005
e-ISSN
1791-7530
Journal
Anticancer Research
Quellenangaben
Volume: 32,
Issue: 10,
Pages: 4251-4261
Publisher
International Institute of Anticancer Research
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501590-001
PubMed ID
23060545
WOS ID
WOS:000310111800008
Erfassungsdatum
2012-11-29