Ethanol-induced ligand-independent activation of ERα mediated by cyclic AMP/PKA signaling pathway: An in vitro study on MCF-7 breast cancer cells

Etique, Nicolas; Flament, Stéphane; Lecomte, J; Grillier-Vuissoz, Isabelle

doi:10.3892/ijo.31.6.1509

Cited by 13 publications

(28 citation statements)

References 51 publications

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“…Treatments were conducted as previously described (19). When ethanol was used as a control, its concentration was 0.1%.…”

Section: Methodsmentioning

confidence: 99%

“…For instance, the mitogen-activated protein kinase (MAPK) pathway activated by epidermal growth factor directly phosphorylates ER· in the absence of ligand and induces ER transactivation (17,18). In MCF-7 breast cancer cells, ethanol induces a ligand-independent activation of ER· mediated by the cAMP/PKA pathway (19). However, the mechanisms involved in the ethanol-induced activation of cAMP/PKA are unknown.…”

Section: Introductionmentioning

confidence: 99%

“…MCF-7 cells were transfected with the expression plasmids using Exgen 500 as recommended by the manufacturer (Euromedex, France). The protocol for transfection experiments has been described previously (19,21). After transfection, cells were allowed to grow for one day and treated for 24 h in fresh medium.…”

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

“…For each gene, the number of cycles was chosen to realize the analysis in the linear phase of the PCR reaction. The PCR products were quantified as previously described (19).…”

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

“…and ß-actin, the protocol for semi-quantitative RT-PCR has been described previously (19,21). The specific primers for A 2A AR were 5'-AACCTGCAGAACGTCACCAA-3' and 5'-GTCACCAAGCCATTGTACCG-3' (22).…”

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

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Crosstalk between adenosine receptor (A2A isoform) and ERα mediates ethanol action in MCF-7 breast cancer cells

Flament¹

2009

Oncol Rep

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Abstract. Alcohol consumption increases the risk of breast cancer but the underlying mechanisms are not well understood. We have shown previously that ethanol activates ER signalling pathway in a cAMP/PKA-mediated ligandindependent manner. Since the activation of A 2A adenosine receptor (A 2A AR) by ethanol has been reported in other cell types, here we tested if cross-talk between this Gs-coupled receptor and ER· could be involved in ethanol effects in breast cancer cells. Our study shows that A 2A AR is expressed and functional in the hormone-dependent breast cancer cell line MCF-7. Interestingly, activation of this receptor by the selective agonist CGS21680 stimulates the transcription of progesterone receptor, a well known estrogen target gene. CGS21680 also stimulates the pEREtkLuc reporter activity in transfected MCF-7 cells, an effect antagonized by the antiestrogen ICI182,780. Moreover, CGS21680 stimulates the proliferation of MCF-7 cells similarly to E 2 . Finally, the A 2A AR antagonist MSX-3 inhibits the ethanol-induced activation of ER· signalling pathway. These results demonstrate cross-talk between A 2A AR and ER· that is involved in ethanol action. This could open new perspectives for the therapy of estrogen-dependent breast cancer.

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“…Treatments were conducted as previously described (19). When ethanol was used as a control, its concentration was 0.1%.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

“…For each gene, the number of cycles was chosen to realize the analysis in the linear phase of the PCR reaction. The PCR products were quantified as previously described (19).…”

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

Section: Semi-quantitative Rt-pcr For Progesterone Receptor (Pr)mentioning

confidence: 99%

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Crosstalk between adenosine receptor (A2A isoform) and ERα mediates ethanol action in MCF-7 breast cancer cells

Flament¹

2009

Oncol Rep

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Short‐term exposure to ethanol induces transcriptional changes in nontumorigenic breast cells

et al. 2023

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Breast cancer is a leading cause of cancer‐related deaths in women. Many genetic and behavioral risk factors can contribute to the initiation and progression of breast cancer, one being alcohol consumption. Numerous epidemiological studies have established a positive correlation between alcohol consumption and breast cancer; however, the molecular basis for this link remains ill defined. Elucidating ethanol‐induced changes to global transcriptional programming in breast cells is important to ultimately understand how alcohol and breast cancer are connected mechanistically. We investigated induced transcriptional changes in response to a short cellular exposure to moderate levels of alcohol. We treated the non‐tumorigenic breast cell line MCF10A, and the tumorigenic breast cell lines MDA‐MB‐231 and MCF7, with ethanol for 6 h, then captured the changes to ongoing transcription using 4‐thiouridine metabolic labeling followed by deep sequencing. Only the MCF10A cell line exhibited statistically significant changes in newly transcribed RNA in response to ethanol treatment. Further experiments revealed that some ethanol‐upregulated genes are sensitive to the dose of alcohol treatment, while others are not. Gene ontology and biochemical pathway analyses revealed that ethanol‐upregulated genes in MCF10A cells are enriched in biological functions that could contribute to cancer development.

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Disruption of ERα signalling pathway by PPARγ agonists: evidences of PPARγ-independent events in two hormone-dependent breast cancer cell lines

Lecomte¹,

Flament²,

Salamone

et al. 2008

Breast Cancer Res Treat

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Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that can be activated by natural ligands such as 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ(2)) as well as synthetic drugs such as thiazolidinediones. The treatment of human breast cancer cell lines with PPARgamma agonists is known to have antiproliferative effects but the role of PPARgamma activation in the process remains unclear. In the present study, we investigated the effects of four PPARgamma agonists, Rosiglitazone (RGZ), Ciglitazone (CGZ), Troglitazone (TGZ) and the natural agonist 15d-PGJ(2), on estrogen receptor alpha (ERalpha) signalling pathway in two hormone-dependent breast cancer cell lines, MCF-7 and ZR-75-1. In both of them, TGZ, CGZ and 15d-PGJ(2) induced an inhibition of ERalpha signalling associated with the proteasomal degradation of ERalpha. ZR-75-1 cells were more sensitive than MCF-7 cells to these compounds. Treatments that induced ERalpha degradation inhibited cell proliferation after 24 h. In contrast, 24 h exposure to RGZ, the most potent activator of PPARgamma disrupted neither ERalpha signalling nor cell proliferation. 9-cis retinoic acid never potentiated the proteasomal degradation of ERalpha. PPARgamma antagonists (T0070907, BADGE and GW 9662) did not block the proteolysis of ERalpha in MCF-7 and ZR-75-1 cells treated with TGZ. ERalpha proteolysis still occurred in case of PPARgamma silencing as well as in case of treatment with the PPARgamma-inactive compound Delta2-TGZ, demonstrating a PPARgamma-independent mechanism. The use of thiazolidinedione derivatives able to trigger ERalpha degradation by a PPARgamma-independent pathway could be an interesting tool for breast cancer therapy.

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Ethanol-induced ligand-independent activation of ERα mediated by cyclic AMP/PKA signaling pathway: An in vitro study on MCF-7 breast cancer cells

Cited by 13 publications

References 51 publications

Crosstalk between adenosine receptor (A2A isoform) and ERα mediates ethanol action in MCF-7 breast cancer cells

Crosstalk between adenosine receptor (A2A isoform) and ERα mediates ethanol action in MCF-7 breast cancer cells

Short‐term exposure to ethanol induces transcriptional changes in nontumorigenic breast cells

Disruption of ERα signalling pathway by PPARγ agonists: evidences of PPARγ-independent events in two hormone-dependent breast cancer cell lines

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