Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Behrens, Diana; Gill, Jason H.; Fichtner, Iduna

doi:10.1016/j.mce.2007.05.012

Cited by 40 publications

(41 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Growth was further inhibited in an estrogen-dependent manner. Other studies support the idea that decreased ERβ expression could lead to breast and ovarian cancer development (15,25,26). Furthermore, ERβ expression in breast cancer cells appears to favor anti-estrogen treatment (24).…”

Section: Discussionmentioning

confidence: 76%

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Feng¹

2011

Oncol Rep

View full text Add to dashboard Cite

Abstract. Ovarian clear cell adenocarcinoma (OCCA) is an aggressive ovarian malignancy with a poor prognosis. The role of estrogen receptor β (ERβ) in the development of OCCA remains to be clarified. To investigate the action of ERβ in the proliferation and invasion of OCCA cells, the ES-2 cell line was stably transfected with full-length human ERβ cDNA, and clones were screened and identified using RT-PCR and Western blot assay. ERβ stable transfectants, referred to as ESβ1 and ESβ2 cells, were compared with mock transfectant ESVE and parental ES-2 cells with respect to their growth, motility and ability to activate target genes. ESβ1 and ESβ2 cells expressed ERβ mRNA and protein, whereas ES-2 and ESVE cells were ERβ negative. ERβ transfectants exhibited distinct characteristics from ES-2 and ESVE cells including proliferative properties and the ability to express cyclin D1 in the presence of 17β-estradiol (E 2 ). ERβ inhibited ES-2 cell proliferation, which was determined using the MTT assay, BrdU labeling method and by the down-regulation of cyclin D1 gene expression. Moreover, exogenous ERβ expression resulted in a significant inhibition of ES-2 cell motility in an in vitro invasion assay. ERβ reduced the expression of MMP2 mRNA and the activity of MMP2 enzymatic activity in a ligand-dependent manner. In summary, ERβ may inhibit the proliferation and invasion of ES-2 cells and may be an important regulator in OCCA carcinogenesis.

show abstract

Section: Discussionmentioning

confidence: 76%

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Feng¹

2011

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Decreased microvessel density and angiogenesis and expression of the proangiogenic factors VEGF and PDGFβ is also observed [72]. ERβ or ERβcx expression in MCF7 cells decreases the percentage of cells in the S phase of the cell cycle [37,71], as well as the number of colonies that grow in soft agar [37].…”

Section: Potential Role Of Erα/erβ Heterodimers In Biological Responsmentioning

confidence: 97%

“…Overexpression of ERβ in ERα+ MCF7 and T47D breast cancer cells inhibits cell proliferation in response to E2 [33,40,70,71], in part by increasing expression of antiproliferative genes (p21 Cip1 and p27 Kip1 ) and decreasing expression of proliferative and antiapoptotic genes (cmyc, cyclin A, and cyclin D1), thus inducing G 2 cell cycle arrest [40,70]. ERβ overexpression also inhibits tumor establishment and growth as well as E2-induced tumor formation in vivo in mouse xenografts of MCF7 and T47D cells [70][71][72]. Decreased microvessel density and angiogenesis and expression of the proangiogenic factors VEGF and PDGFβ is also observed [72].…”

Section: Potential Role Of Erα/erβ Heterodimers In Biological Responsmentioning

confidence: 99%

ERβ in breast cancer—Onlooker, passive player, or active protector?

2008

View full text Add to dashboard Cite

The role of estrogen exposure in breast cancer risk is well-documented, and both estrogen synthesis and actions through the estrogen receptor (ER) have been targeted by therapies to control hormonedependent breast cancer. The discovery of a second ER form and its therapeutic implications sparked great interest. Both the original ERα and the more recently identified ERβ subtypes bind and respond similarly to many physiological and pharmacological ligands. However, differences in phytoestrogen binding have been noted, and subtype-specific ligands have been developed. Cell-based assays show that ERβ and its variants are generally less active on gene transcription than ERα, and may influence ERα activity; however, both gene-and cell-specific responses occur, and nongenomic activities are less well explored. Specific ligands, and methods to disrupt or eliminate receptor subtype expression in animal and cell models, demonstrate that the ERs have both overlapping and distinct biological functions. Overall, in cell-based studies, ERα appears to play a predominant role in cell proliferation, and ERβ is suggested to be antiproliferative.The potential for distinct populations of breast tumors to be identified based on ER subtype expression, and to exhibit distinct clinical behaviors, is of greatest interest. Several studies suggest that the majority of ER-positive tumors contain both subtypes, but that some tumors contain only ERβ and may have distinct clinical behaviors and responses. Expression of ERβ together with ERα favors positive responses to endocrine therapy in most studies, and additional studies to determine if the addition of ERβ to ERα as a tumor marker is of clinical benefit are warranted. In contrast, the positive association between ERβ and HER2 expression in high-grade ERα-negative breast cancer does not favor positive responses to endocrine therapy. Expression of ERβ in specific clinical subpopulations, and the potential for therapies targeting ERβ specifically, is discussed.

show abstract

“…High ERb expression in MCF-7 cell cultures has been shown to inhibit E2-dependent 59 and independent proliferation. 60 Enterolignans have been documented to have cytostatic properties on cell cycle and proliferation in rat hepatomas 61 and human colon cancer xenografts, 62 but we did not find any effect of lariciresinol on expression of tumor proliferation marker Ki-67 in MCF-7 xenografts.…”

Section: Discussionmentioning

confidence: 99%

Dietary lariciresinol attenuates mammary tumor growth and reduces blood vessel density in human MCF‐7 breast cancer xenografts and carcinogen‐induced mammary tumors in rats

Saarinen

Wärri

Dings

et al. 2008

Intl Journal of Cancer

View full text Add to dashboard Cite

Lariciresinol is a dietary lignan that accounts for a significant portion of the total phytoestrogen intake from Western foods. Recent epidemiological studies suggest that high dietary intake of lignans and lariciresinol is associated with reduced breast cancer risk. However, no causal relationship between lariciresinol intake and breast cancer development has been established. In this study, we investigated for the first time the effects and possible mechanisms of action of lariciresinol on hormone responsive mammary cancer in vivo in dimethylbenz [a]anthracene induced mammary cancer in rats, and in human MCF-7 breast cancer xenografts in athymic mice. For tumor bearing rats, lariciresinol (3 or 15 mg/kg of body weight) or vehicle was administered p.o. daily for 9 weeks. For E2-maintained ovariectomized athymic mice bearing orthotopic MCF-7 tumors, control diet (AIN-93G) or lariciresinol containing diet (AIN-93G supplemented with 20 or 100 mg of lariciresinol/kg of diet) was administered for 5 weeks. In both models, lariciresinol administration inhibited the tumor growth and tumor angiogenesis. In MCF-7 cells, enterolactone significantly inhibited the E2-stimulated VEGF secretion. Moreover, in MCF-7 xenografts, lariciresinol administration enhanced tumor cell apoptosis and increased estrogen receptor beta expression. Lariciresinol and its further metabolites secoisolariciresinol, enterodiol and enterolactone were found in serum of both rats and athymic mice confirming a similar lignan metabolism pattern as in humans. These findings indicate conceivable importance of dietary lignan lariciresinol in inhibition of breast cancer development.

show abstract

Loss of tumourigenicity of stably ERβ-transfected MCF-7 breast cancer cells

Cited by 40 publications

References 59 publications

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

Re-expression of estrogen receptor β inhibits the proliferation and migration of ovarian clear cell adenocarcinoma cells

ERβ in breast cancer—Onlooker, passive player, or active protector?

Dietary lariciresinol attenuates mammary tumor growth and reduces blood vessel density in human MCF‐7 breast cancer xenografts and carcinogen‐induced mammary tumors in rats

Contact Info

Product

Resources

About