The oestrogen receptor modulates growth of pituitary tumour cells in the absence of exogenous oestrogen

Newton, C. J.; Trapp, Thorsten; Pagotto, Uberto; Renner, Ulrich; Buric, Rosa; Stalla, Günter

doi:10.1677/jme.0.0120303

Cited by 16 publications

(5 citation statements)

References 41 publications

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“…This stimulation was blocked by an anti-oestrogen suggesting that IGF-1 was acting on a component of the ER pathway. In the absence of any E 2 , Newton et al (1994) also observed stimulation of ER-mediated reporter-gene activity by IGF-1 in the pituitary tumour cell line, GH 3 . The mechanism of this ligand-independent activation of the ER is still unclear but it may be involved in the development of tamoxifen resistance.…”

mentioning

confidence: 82%

Altered expression of the IGF-1 receptor in a tamoxifen-resistant human breast cancer cell line

Parisot

Deluise

et al. 1999

Br J Cancer

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SummaryThe relationship between oestrogen (E 2 ) and insulin-like growth factor-one (IGF-1) was examined in both tamoxifen-sensitive (MCF 7/5-21) and tamoxifen-resistant (MCF 7/5-23) subclones of the MCF 7 cell line. Both subclones were grown in defined, serum-free (SF) medium over a period of 7 days with the addition of E 2 or IGF-1 or a combination of both agents. Growth of both MCF 7/5-21 and 7/5-23 cells was stimulated (245% and 350%, respectively) by E 2 . However, only the growth of MCF 7/5-23 cells was stimulated (266%) by IGF-1. A combination of E 2 and IGF-1 significantly enhanced MCF 7/5-21 and 7/5-23 cell growth (581% and 695%, respectively). E 2 -induced IGF-1 receptor (IGF-1R) levels (as measured by 125 I-IGF-1 binding and Northern analyses) in only MCF 7/5-23 cells. This effect was partially inhibited by tamoxifen. In medium containing serum, the growth of only the MCF 7/5-23 cells was significantly inhibited by the IGF-1R monoclonal antibody, αIR-3. The detection of E 2 -induced expression of IGF-2 using RT-PCR was demonstrated in the MCF 7/5-23 cells. These experiments indicate that E 2 may sensitize tamoxifen-resistant MCF 7/5-23 cells to the growth stimulatory actions of IGF-2 via upregulation of the IGF-1R and describes a cell-survival mechanism that may manifest itself as tamoxifen resistance.

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confidence: 82%

Altered expression of the IGF-1 receptor in a tamoxifen-resistant human breast cancer cell line

Parisot

Deluise

et al. 1999

Br J Cancer

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“…Because vascular endothelial cells were not found to express the β-subunits of the channels [36], it is tempting to speculate that the BK Ca channel, where little or no β-subunits are co-expressed, is subject to inhibition by ICI-182,780. ICI-182,780 was also reported to suppress the growth of pituitary tumor cells and endothelial cells [35,37]. The BK Ca channel has been recently demonstrated to be presumably associated with growth control in human glioma cells [38].…”

Section: Ici-182780mentioning

confidence: 99%

Pharmacological Roles of the Large-Conductance Calcium-Activated Potassium Channel

Wu¹,

Wu²,

Lin³

2006

CTMC

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The gating of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channel is primarily controlled by intracellular Ca(2+) and/or membrane depolarization. These channels play a role in the coupling of excitation-contraction and stimulus-secretion. A variety of structurally distinct compounds may influence the activity of these channels. Squamocin, an Annonaceous acetogenin, could interact with the BK(Ca) channel to increase the amplitude of Ca(2+)-activated K(+) current in coronary smooth muscle cells. Its stimulatory effect is related to intracellular Ca(2+) concentrations. In inside-out patches, application of ceramide to the bath suppressed the activity of BK(Ca) channels recorded from pituitary GH(3) cells and from retinal pigment epithelial cells. ICI-182,780, an estrogen receptor antagonist, was found to modulate BK(Ca)-channel activity in cultured endothelial cells and smooth muscle cells in a mechanism unlinked to the inhibition of estrogen receptors. Caffeic acid phenethyl ester (CAPE) and its analogy, cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate, could directly increase the activity of BK(Ca) channels in GH(3) cells. CAPE also reduced the frequency and amplitude of intracellular Ca(2+) oscillations in these cells. The CAPE-stimulated activity in BK(Ca) channels is thought to be unassociated with its inhibition of NF-kappaB activation. Cilostazol, an inhibitor of cyclic nucleotide phosphodiesterase, could stimulate BK(Ca) channel-activity and reduce the firing of action currents simultaneously in GH(3) cells. Therefore, the regulation by these compounds of BK(Ca) channels may in part be responsible for their regulatory actions on cell functions.

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“…An inhibition of protein kinase (PK) A, PKC and MAP kinase pathways also down-regulated IL-6induced reporter gene activity (Hobisch et al, 1998), however, inhibitors of PKC failed to block growth factor-dependent activation, suggesting multiple pathways for ligand-independent activation of ERα (Ignar-Trowbridge et al, 1996). Other examples of ligand-independent activation of ERα include IL-2 and insulinlike growth factor (IGF)-I (Newton et al, 1994a(Newton et al, , 1994b.…”

Section: mentioning

confidence: 99%

“…IL-6 is one such factor (Speirs et al, 1993;Duncan et al, 1994). There is evidence for cross-talk between ERα and growth factors with direct activation of ERα in response to IL-2 (Newton et al, 1994a) and IGF-I (Newton et al, 1994b;Lee et al, 1997) in ERα-positive breast and pituitary cell lines. Related to these observations, IL-6 has recently been shown to activate the androgen receptor in another hormone-sensitive cancer, prostate cancer (Hobisch et al, 1998).…”

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confidence: 99%

Direct activation of oestrogen receptor- α by interleukin-6 in primary cultures of breast cancer epithelial cells

et al. 2000

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Interleukin 6 (IL-6) is secreted by breast tumours and shows synergistic activity with 17β-oestradiol (E2), leading to increases in reductive 17β-hydroxysteroid dehydrogenase activity in breast cancer epithelial cells. However, the mechanisms involved are poorly understood. Using short-term epithelial cultures established from primary breast tumours, we have examined whether IL-6 could directly affect transcriptional activity of oestrogen reception α (ERα). Tumour epithelial cultures were established from 15 breast tumours, grown to 70% confluence and transiently transfected with a plasmid reporter containing the vitellogenin oestrogen response element and the luciferase coding sequence (ERE-TK-LUC). Following transfection, cells were incubated with E2, IL-6, the pure anti-oestrogen ZM 182780 or combinations of these substances for 48 h. Luciferase activity was then measured in cell lysates. E2 caused a dose-dependent increase in luciferase expression, causing a maximum threefold stimulation at 100 p M. In the presence of IL-6, transcriptional activity was increased by up to 2.5-fold in ERα+cultures (11/15). In combination with E2, synergistic effects were observed with increases in luciferase activity of up to sixfold over controls. This effect could be blocked by treatment with ZM 182780. Pre-incubation of cells with an antibody directed against the signalling component of IL-6, gp130, was ineffective in blocking the E2 response. This antibody reduced, but did not completely block the effect of IL-6 either alone or in combination with E2, suggesting cross-talk between the two signalling pathways. In conclusion, these results provide evidence for direct transcriptional activation of ERα by IL-6. © 2000 Cancer Research Campaign

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The oestrogen receptor modulates growth of pituitary tumour cells in the absence of exogenous oestrogen

Cited by 16 publications

References 41 publications

Altered expression of the IGF-1 receptor in a tamoxifen-resistant human breast cancer cell line

Altered expression of the IGF-1 receptor in a tamoxifen-resistant human breast cancer cell line

Pharmacological Roles of the Large-Conductance Calcium-Activated Potassium Channel

Direct activation of oestrogen receptor- α by interleukin-6 in primary cultures of breast cancer epithelial cells

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