Glucocorticoid-mediated inhibition of chemotherapy in ovarian carcinomas

Zhang, Chengwen; Marmé, Alexander; Wenger, Till; Gutwein, Paul; Edler, Lutz; Rittgen, Werner; Debatin, Klaus‐Michael; Altevogt, Peter; Mattern, J; Herr, Ingrid

doi:10.3892/ijo.28.2.551

Cited by 33 publications

(38 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The results of Wang et al 87 however, can not be explained on the basis of cell kinetics. Thus, the results from our 6,90,91,95 and other studies in murine and human tumor xenografts indicate that, in GC-sensitive tumors, concurrent treatment with steroids and anticancer drugs may be contraindicated and that the effectiveness of cycle stage-specific agents may be considerably reduced due to unfavorable cell cycle distributions. On the other hand, GCs may add significantly to the effectiveness of a sequential chemotherapy program when used appropriately by altering the temporal relationship of the recovery events in the tumor and the normal tissues.…”

Section: © 2 0 0 8 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 71%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

Self Cite

View full text Add to dashboard Cite

ABBrevIAtIons DEX ABstrActGlucocorticoids have been widely used as cotreatment for patients with cancer due to potent pro-apoptotic properties in lymphoid cells, reduction of nausea and diminishing acute toxicity on normal tissue. There are now data from preclinical and, to some extent, clinical studies, demonstrating that these medicaments are highly suspicious to induce therapy resistance in the majority of malignant solid tumors-irrespective of tumor origin and the nature of specific anticancer drugs or irradiation used for treatment. Despite these huge amounts of data, the underlying mechanisms of cell type-specific signaling by these steroid hormones are just beginning to be described. This review summarizes our present understanding of a relationship between glucocorticoid-induced reversible cell cycle arrest and therapy resistance in solid tumors. We give a summary of our current knowledge of decreased proliferation rates in response to glucocorticoid pre and combination treatment which are suspicious to be involved not only in protection of normal tissues, but also in protection of solid tumors from cytotoxic effects of anticancer agents. The inhibition of cell cycle progression by pretreatment with GCs may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with GCs.

show abstract

Section: © 2 0 0 8 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 71%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

Self Cite

View full text Add to dashboard Cite

show abstract

“…A recent study reported that the systemic administration of steroids reduced chemotherapy-induced adverse effects; however, they also reduced the tumoricidal activity of the chemotherapy (Zhang et al, 2006). This limits the systemic use of steroids and favors a local administration of such drugs.…”

Section: Discussionmentioning

confidence: 99%

“…However, some agents that protect hearing reduce antitumor efficacy (Zhang et al, 2006). A recent study reported that the systemic administration of steroids reduced chemotherapy-induced adverse effects; however, they also reduced the tumoricidal activity of the chemotherapy (Zhang et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

et al. 2010

View full text Add to dashboard Cite

“…Be ca use of the pro-apoptotic and anti-proliferative effects in lymphoid tissues, GCs, such as the highly effec tive synt hetic agent dexamethasone (DEX), are widely used as co-medication in cancer therapy (9). The distinct effects of GCs on different tumor types have been reported.…”

Section: Introductionmentioning

confidence: 99%

“…The distinct effects of GCs on different tumor types have been reported. Contrary to the supportive action of GCs in the anti-tumor therapy of lymphomas, glucocorticoid-induced resistance toward cancer therapy is common in ova rian, lung and cervical carcinomas (9,10). A possi ble involvement of GCs in the regulation of gal-1 expression in choriocarcinoma cells has not been studied so far.…”

Section: Introductionmentioning

confidence: 99%

Choriocarcinoma cell line Response to Dexamethasone

Bojić‐Trbojević¹,

Kolundžić²,

Petronijević³

et al. 2010

Journal of Medical Biochemistry

View full text Add to dashboard Cite

Kratak sadr`aj: Horiokarcinomske }elijske linije JAr i JEG-3 su model sistemi za ispitivanje transformisanog trofo blasta. Obe }elijske linije eksprimiraju galektin-1, ~ija je pove}ana ekspresija pokazana u horiokarcinomima u odno su na normalni trofoblast trudno}e. U ovom radu ispitivan je efekat sintetskog glukokortikoida deksametazona na JAr i JEG-3 }elijske linije, upotrebom MTT testa, ELISA testa na }elijama i testovima adhezije i migracije. Broj `ivih }elija, kao indikator proliferacije }elija, zna ~ajno je pove}an nakon tretmana 0,1 i 1 nmol/L deksameta zonom, a proliferacija JEG-3 je zna~ajno pove}ana u ~itavom opsegu upotrebljenih koncentracija deksameta zo na (0,1-100 nmol/L). Galektin-1 je u JAr moduliran deksametazonom, koji blago, ali zna~ajno smanjuje pro duk ciju galektina-1 u niskim koncentracijama (0,1 i 1 nmol/L). Kod JEG-3 }elija, produkcija galektina-1 je zna~ajno smanjena samo nakon tretmana 100 nmol/L deksameta zonom. U prisustvu laktoze kao inhibitornog {e}era za galektin-1 adhezija JEG-3 }elija je zna~ajno pove}ana, dok deksa metazon uz to smanjuje i migraciju JEG-3 }elija. Rezultati dobijeni u ovom radu po kazuju da deksametazon uti~e na proliferaciju i u manjoj meri na galektin-1 kod JAr i JEG-3 }elija, na na~in spe ci fi~an za }elijsku liniju. Dobijeni podaci ukazuju na to da bi tret man glukokortikoidima in vivo mogao imati uticaja na }elije horiokarcinoma. Summary: Choriocarcinoma cell lines JAr and JEG-3 are model systems for the study of transformed trophoblast. Both cell lines were shown to produce galectin-1, expression of which was increased in choriocarcinoma when compared to the normal trophoblast of pregnancy. In this study the effects of synthetic glucocorticoid dexamethasone were inves ti gated in both JAr and JEG-3 cell lines by the MTT test, cell based ELISA, and the cell adhesion and migration tests. Viable cell number/cell proliferation of JAr cells was signi ficantly increased after treatment with 0.1 and 1 nmol/L of dexamethasone, while proliferation of JEG-3 cells was signi ficantly increased after treatment in the whole concentration range of dexamethasone (0.1-100 nmol/L). Galectin-1 in JAr cells was modulated by dexamethasone, which mildly, but significantly decreased production at low concentrations (0.1 and 1 nmol/L). In JEG-3 cells pro duction of galectin-1 was significantly decreased only after treat ment with 100 nmol/L of dexamethasone. Cell adhe sion of JEG-3 was significantly increased in the presence of lacto se, an inhibitory sugar for gal-1, while dexamethasone indu ced decrease of JEG-3 cell migration. These findings have shown that dexamethasone may affect proliferation, gal-1 production and cell migration, in a cell line specific manner. These data suggest that glucocorticoid treatment in vivo might have the potential to affect cell functions in cho riocarcinoma.

show abstract

Glucocorticoid-mediated inhibition of chemotherapy in ovarian carcinomas

Cited by 33 publications

References 17 publications

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

Choriocarcinoma cell line Response to Dexamethasone

Contact Info

Product

Resources

About