We are analyzing https://link.springer.com/article/10.1007/s10549-010-1273-5.

Title:
Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2 | Breast Cancer Research and Treatment
Description:
The role of estrogen receptor beta (ERβ) in breast cancer is unclear. ERβ is considered to have a protective role in breast cancer development based on findings demonstrating that ERβ expression inhibits ERα-mediated proliferation of breast cancer cells. We previously demonstrated that ERβ causes a ligand independent G2 cell cycle arrest in MCF-7 cells. To study the mechanisms of the ERβ-mediated G2 cell cycle arrest, we investigated its effects on the regulatory pathways responsible for the G2/M phase transition. We found that ERβ inhibits CDK1 activity, which is the critical determinant of the G2/M progression. CDK1 activity is modulated by both stimulatory and inhibitory factors. Cyclin B1 is the major activator of CDK1. ERβ inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein. GADD45A and BTG2 are two major inhibitors of CDK1, which have been implicated in breast tumor formation. Based on these findings, we explored if the expression pattern of GADD45A and BTG2 is affected by ERβ. We found that ERβ stimulates GADD45A and BTG2 mRNA levels. The induction of these two genes is caused by ERβ binding directly to these genes and recruiting c-jun and NCOA2. Our findings demonstrated that unliganded ERβ causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression. These results provide evidence that drugs that stimulate the production of unliganded ERβ may be effective new therapies to prevent breast cancer.
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Keywords {🔍}

article, google, scholar, cancer, pubmed, cas, breast, cell, estrogen, receptor, beta, erβ, expression, btg, cells, res, cycle, arrest, cyclin, gadda, cdk, regulation, inhibits, protein, biol, research, activity, paruthiyil, leitman, human, usa, privacy, cookies, content, proliferation, genes, binding, access, receptors, oncogene, gene, mammalian, transcriptional, analysis, publish, search, treatment, cvoro, dale, role,

Topics {✒️}

nf-kappab-responsive gene btg2 month download article/chapter β-arrestins inhibits proliferation estrogen receptor-beta evaluation cell cycle-dependent usage gadd45-mediated growth suppression cell cycle-dependent stimulation cell cycle-dependent regulation mammalian cell-cycle regulation antiproliferative p53-dependent component estrogen receptor beta estrogen receptor β mcf-7 cells estrogen receptor pathways frequently methylated gene p53-regulated protein gadd45 fornace aj jr er-beta expression isaac cohen & emma shtivelman breast cancer cells growth arrest signals human breast cancer full article pdf hormone binding domains pkc-delta pathway liganded estrogen receptors privacy choices/manage cookies breast tumor formation related subjects guerra-vladusic fk normal human fibroblasts prevent breast cancer primary breast cancer cdc2 kinase correlates dna-damaging agents estrogen receptor btg2 mrna levels tis21/btg2/pc3 received financial support cyclin-kinase inhibitors cyclin b1 promoter american cancer society erβ stimulates gadd45a erβ binding directly olson ja jr european economic area regulatory pathways responsible recruiting c-jun results provide evidence check access

Schema {🗺️}

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         headline:Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2
         description:The role of estrogen receptor beta (ERβ) in breast cancer is unclear. ERβ is considered to have a protective role in breast cancer development based on findings demonstrating that ERβ expression inhibits ERα-mediated proliferation of breast cancer cells. We previously demonstrated that ERβ causes a ligand independent G2 cell cycle arrest in MCF-7 cells. To study the mechanisms of the ERβ-mediated G2 cell cycle arrest, we investigated its effects on the regulatory pathways responsible for the G2/M phase transition. We found that ERβ inhibits CDK1 activity, which is the critical determinant of the G2/M progression. CDK1 activity is modulated by both stimulatory and inhibitory factors. Cyclin B1 is the major activator of CDK1. ERβ inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein. GADD45A and BTG2 are two major inhibitors of CDK1, which have been implicated in breast tumor formation. Based on these findings, we explored if the expression pattern of GADD45A and BTG2 is affected by ERβ. We found that ERβ stimulates GADD45A and BTG2 mRNA levels. The induction of these two genes is caused by ERβ binding directly to these genes and recruiting c-jun and NCOA2. Our findings demonstrated that unliganded ERβ causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression. These results provide evidence that drugs that stimulate the production of unliganded ERβ may be effective new therapies to prevent breast cancer.
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            Gene expression
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      headline:Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2
      description:The role of estrogen receptor beta (ERβ) in breast cancer is unclear. ERβ is considered to have a protective role in breast cancer development based on findings demonstrating that ERβ expression inhibits ERα-mediated proliferation of breast cancer cells. We previously demonstrated that ERβ causes a ligand independent G2 cell cycle arrest in MCF-7 cells. To study the mechanisms of the ERβ-mediated G2 cell cycle arrest, we investigated its effects on the regulatory pathways responsible for the G2/M phase transition. We found that ERβ inhibits CDK1 activity, which is the critical determinant of the G2/M progression. CDK1 activity is modulated by both stimulatory and inhibitory factors. Cyclin B1 is the major activator of CDK1. ERβ inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein. GADD45A and BTG2 are two major inhibitors of CDK1, which have been implicated in breast tumor formation. Based on these findings, we explored if the expression pattern of GADD45A and BTG2 is affected by ERβ. We found that ERβ stimulates GADD45A and BTG2 mRNA levels. The induction of these two genes is caused by ERβ binding directly to these genes and recruiting c-jun and NCOA2. Our findings demonstrated that unliganded ERβ causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression. These results provide evidence that drugs that stimulate the production of unliganded ERβ may be effective new therapies to prevent breast cancer.
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      dateModified:2010-12-01T00:00:00Z
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         Estrogen receptor
         Breast cancer
         Gene expression
         Cell cycle
         GADD45A
         BTG2
         MCF-7 cells
         Oncology
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