Glucocorticoid receptors and growth inhibitory effects of dexamethasone in human lung cancer cell lines

Hofmann, Jürgen; Kaiser, Ulrich; Maasberg, Michael; Havemann, K.

doi:10.1016/0959-8049(95)00431-9

Cited by 36 publications

(28 citation statements)

References 21 publications

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“…By extending earlier observations, we have shown that human SCLC cells are profoundly resistant to Gc action, due to deficient GR expression. A correlation between decreased GR expression and resistance to the antiproliferative effects of Gc in human small cell carcinoma has been noted before, but the mechanism has not been explored (Hofmann et al, 1995). In solid tumour models, a correlation between GR content and Gc sensitivity has also been described (Braunschweiger et al, 1983).…”

Section: Discussionmentioning

confidence: 95%

Glucocorticoid receptor overexpression exerts an antisurvival effect on human small cell lung cancer cells

et al. 2007

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Section: Discussionmentioning

confidence: 95%

Glucocorticoid receptor overexpression exerts an antisurvival effect on human small cell lung cancer cells

et al. 2007

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“…The growth-inhibitory effect of Dex plus vesnarinone was observed in all of the NSCLC cells tested. A significant incidence of specific, high-affinity receptors for glucocorticoids is present in NSCLC (Chaudhuri et al, 1982;Beattie et al, 1985;Hofmann et al, 1995). The growth of approximately one-third of the NSCLC cell lines was inhibited by Dex, although the growth-inhibitory effect was modest in most of the cell lines (Hofmann et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…A significant incidence of specific, high-affinity receptors for glucocorticoids is present in NSCLC (Chaudhuri et al, 1982;Beattie et al, 1985;Hofmann et al, 1995). The growth of approximately one-third of the NSCLC cell lines was inhibited by Dex, although the growth-inhibitory effect was modest in most of the cell lines (Hofmann et al, 1995). Glucocorticoids can be administered to patients with NSCLC with tolerable side-effects, although the steroids alone have no anticancer effect in lung cancer patients.…”

Section: Discussionmentioning

confidence: 99%

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

1999

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Vesnarinone, an oral cardiotonic, inhibited the growth of several human non-small cell lung carcinoma cell lines, and its anti-proliferative effects in vitro and in vivo were greatly enhanced by combination with glucocorticoids, but not other steroids. Simultaneous treatment with vesnarinone and dexamethasone is the most effective to evoke the synergistic effect in the growth inhibition of lung carcinoma EBC-1 cells. Dexamethasone and other glucocorticoids induced morphological changes in EBC-1 cells and these agents together with vesnarinone induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. This treatment arrested the growth of the cells at the G 1 phase, indicating that this treatment is cytostatic rather than cytotoxic. These results suggest that vesnarinone plus glucocorticoid might be useful in lung cancer therapy. © 1999 Cancer Research Campaign

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“…The authors demonstrated that the GR content of cell lines in which DEX blocked cell cycle progression was significantly higher than in those cell lines unaffected by DEX. Hofmann et al 25 found that human lung cancer cell lines responsive to DEX had higher GR concentrations than nonresponders. The growth-inhibitory effect of DEX could be blocked by the GR antagonist RU-486.…”

Section: The Effect Of Gcs Is Dependent On Gr Levelsmentioning

confidence: 99%

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

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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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.

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Glucocorticoid receptors and growth inhibitory effects of dexamethasone in human lung cancer cell lines

Cited by 36 publications

References 21 publications

Glucocorticoid receptor overexpression exerts an antisurvival effect on human small cell lung cancer cells

Glucocorticoid receptor overexpression exerts an antisurvival effect on human small cell lung cancer cells

Vesnarinone and glucocorticoids cooperatively induce G1 arrest and have an anti-tumour effect on human non-small cell lung carcinoma cells grown in nude mice

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

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