PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3666278-4 1987 The addition of varying concentrations of retinoic acid (RA) to varying concentrations of tamoxifen (TMX) resulted in an additive effect on the inhibition of proliferation of the ER-positive human carcinoma cell lines (MCF-7). Tretinoin 42-55 estrogen receptor 1 Homo sapiens 179-181 34389675-5 2021 There were two unexpected findings: 1) a strong induction of CYPs involved in activation of fatty acids (CYP4), and in inactivation of calcitriol (CYP24A1) and retinoic acid (CYP26A1); and 2) a marked down-regulation of FOS, FRA1, and JUN, known tethering partners of ERbeta. Tretinoin 160-173 estrogen receptor 1 Homo sapiens 268-274 2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 132-149 2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 151-153 2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 15-17 estrogen receptor 1 Homo sapiens 132-149 2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 15-17 estrogen receptor 1 Homo sapiens 151-153 2317786-2 1990 RA inhibition of human breast carcinoma cell proliferation is associated with marked inhibition of the synthesis of a Mr 39,000 protein in the ER-positive human breast carcinoma cell lines investigated. Tretinoin 0-2 estrogen receptor 1 Homo sapiens 143-145 29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 61-68 32323852-5 2020 In addition, through transient expression assays in breast cancer cells, it was revealed that a transcriptional mechanism dependent on protein kinase A and susceptible to retinoic acid in ER-positive cells induces GPR30 expression through a cis-regulatory element for E26 transformation-specific transcription factors, located between -631 and -625 bp from the GPR30 translation start codon. Tretinoin 171-184 estrogen receptor 1 Homo sapiens 188-190 29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 95-102 29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 95-102 29447503-5 2018 To do so, this study assessed the effects of AtRA on different ERalpha-related events such as ERalpha-mediated cell proliferation and gene expression, ERalpha-coregulator binding and ERalpha subcellular localization. Tretinoin 45-49 estrogen receptor 1 Homo sapiens 63-70 29447503-8 2018 Interestingly, in the absence of E2, ERalpha-mediated gene expression, ERalpha-coregulator binding and ERalpha subcellular mobilization were increased upon exposure to micromolar concentrations of AtRA found to inhibit cell proliferation after long-term exposure. Tretinoin 197-201 estrogen receptor 1 Homo sapiens 37-44 29447503-8 2018 Interestingly, in the absence of E2, ERalpha-mediated gene expression, ERalpha-coregulator binding and ERalpha subcellular mobilization were increased upon exposure to micromolar concentrations of AtRA found to inhibit cell proliferation after long-term exposure. Tretinoin 197-201 estrogen receptor 1 Homo sapiens 71-110 29447503-9 2018 Nevertheless, experiments using purified ERalpha showed that direct binding of AtRA to ERalpha does not occur. Tretinoin 79-83 estrogen receptor 1 Homo sapiens 87-94 20300827-2 2011 Recently, we reported significant stimulation of all-trans retinoic acid (atRA)-induced NIS expression in the estrogen-receptor positive human breast cancer cell line MCF-7 by dexamethasone (Dex) in vitro and in vivo, which might offer the potential to image and treat breast cancer with radioiodine. Tretinoin 53-72 estrogen receptor 1 Homo sapiens 110-127 26379840-6 2015 It appeared that retinoic acid nanoparticle conjugates were selectively taken and retained by the estrogen receptor alpha present in the plasma membrane. Tretinoin 17-30 estrogen receptor 1 Homo sapiens 98-121 23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 estrogen receptor 1 Homo sapiens 243-266 23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 estrogen receptor 1 Homo sapiens 268-275 20300827-2 2011 Recently, we reported significant stimulation of all-trans retinoic acid (atRA)-induced NIS expression in the estrogen-receptor positive human breast cancer cell line MCF-7 by dexamethasone (Dex) in vitro and in vivo, which might offer the potential to image and treat breast cancer with radioiodine. Tretinoin 74-78 estrogen receptor 1 Homo sapiens 110-127 18692045-10 2008 There is thus a membrane localized estrogen receptor in HL-60 myeloblastic leukemia cells that can cause ERK activation and modulates the response of these cells to retinoic acid, indicating crosstalk between the membrane estrogen and retinoic acid evoked pathways relevant to propulsion of cell differentiation. Tretinoin 165-178 estrogen receptor 1 Homo sapiens 35-52 20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 77-90 estrogen receptor 1 Homo sapiens 13-15 20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 92-96 estrogen receptor 1 Homo sapiens 13-15 18692045-10 2008 There is thus a membrane localized estrogen receptor in HL-60 myeloblastic leukemia cells that can cause ERK activation and modulates the response of these cells to retinoic acid, indicating crosstalk between the membrane estrogen and retinoic acid evoked pathways relevant to propulsion of cell differentiation. Tretinoin 235-248 estrogen receptor 1 Homo sapiens 35-52 17591692-0 2007 The silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressor is required for full estrogen receptor alpha transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 109-132 15713534-2 2005 The silencing mediator of retinoic acid and thyroid hormone (SMRT) and other members of the corepressor complex are enriched in spherical intranuclear foci, and repress estrogen receptor alpha (ERalpha)-dependent transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 169-192 16740359-2 2007 This study investigates the individual and combined effects of PML, when overexpressed by the recombinant PML adenovirus, and all-trans-retinoic acid on the proliferation of human estrogen-receptor negative SKBR-3 and estrogen-receptor positive MCF-7 breast cancer cell lines. Tretinoin 126-149 estrogen receptor 1 Homo sapiens 180-197 16740359-2 2007 This study investigates the individual and combined effects of PML, when overexpressed by the recombinant PML adenovirus, and all-trans-retinoic acid on the proliferation of human estrogen-receptor negative SKBR-3 and estrogen-receptor positive MCF-7 breast cancer cell lines. Tretinoin 126-149 estrogen receptor 1 Homo sapiens 218-235 17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 87-100 estrogen receptor 1 Homo sapiens 152-175 17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 87-100 estrogen receptor 1 Homo sapiens 177-184 17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 102-104 estrogen receptor 1 Homo sapiens 152-175 17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 102-104 estrogen receptor 1 Homo sapiens 177-184 17387344-6 2007 Retinoic acid metabolism blocking agents induced cell differentiation as determined by increased expression of cytokeratin 8/18 and oestrogen receptor-alpha (ER-alpha). Tretinoin 0-13 estrogen receptor 1 Homo sapiens 158-166 15713534-2 2005 The silencing mediator of retinoic acid and thyroid hormone (SMRT) and other members of the corepressor complex are enriched in spherical intranuclear foci, and repress estrogen receptor alpha (ERalpha)-dependent transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 194-201 12080040-1 2002 All-trans-retinoic acid has been shown to have an antiproliferative effect in the estrogen receptor alpha-positive breast cancer cell line MCF-7. Tretinoin 0-23 estrogen receptor 1 Homo sapiens 82-105 15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 54-67 estrogen receptor 1 Homo sapiens 12-29 15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 54-67 estrogen receptor 1 Homo sapiens 31-33 15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 69-71 estrogen receptor 1 Homo sapiens 12-29 15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 69-71 estrogen receptor 1 Homo sapiens 31-33 12943740-2 2003 We have previously shown that re-expression of ERalpha in ER-negative cells stimulates the transcriptional and growth inhibitory effects of all-trans-retinoic acid (tRA) by a mechanism that is independent of the ER ligands estradiol and tamoxifen. Tretinoin 140-163 estrogen receptor 1 Homo sapiens 47-54 12943740-2 2003 We have previously shown that re-expression of ERalpha in ER-negative cells stimulates the transcriptional and growth inhibitory effects of all-trans-retinoic acid (tRA) by a mechanism that is independent of the ER ligands estradiol and tamoxifen. Tretinoin 165-168 estrogen receptor 1 Homo sapiens 47-54 12080040-11 2002 This finding indicates that Hairy and Enhancer of Split homologue-1 is a mediator of the antiproliferative effect of all-trans-retinoic acid in estrogen receptor alpha-positive breast cancer cell lines. Tretinoin 117-140 estrogen receptor 1 Homo sapiens 144-167 9823320-5 1998 However, stable expression of ER increased retinoid activation of transcription of a retinoic acid (RA) response elements from the low level in MDA-MB-231 to approach the level of MCF-7. Tretinoin 85-98 estrogen receptor 1 Homo sapiens 30-32 11836298-0 2002 Divergent effects of retinoic acids on the expression of ERalpha and 17beta-hydroxysteroid dehydrogenase type 2 in endometrial carcinoma cells (RL 95-2). Tretinoin 21-35 estrogen receptor 1 Homo sapiens 57-64 10965999-1 2000 It has been established that melatonin (Mlt) and retinoic acid, individually, inhibit the proliferation of the estrogen receptor-alpha (ER alpha)-positive MCF-7 breast cancer cell line. Tretinoin 49-62 estrogen receptor 1 Homo sapiens 111-134 10965999-1 2000 It has been established that melatonin (Mlt) and retinoic acid, individually, inhibit the proliferation of the estrogen receptor-alpha (ER alpha)-positive MCF-7 breast cancer cell line. Tretinoin 49-62 estrogen receptor 1 Homo sapiens 136-144 9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 82-95 estrogen receptor 1 Homo sapiens 13-30 9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 82-95 estrogen receptor 1 Homo sapiens 32-34 9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 97-99 estrogen receptor 1 Homo sapiens 13-30 9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 97-99 estrogen receptor 1 Homo sapiens 32-34 9892191-3 1999 Western blot analysis showed that tyrosine phosphorylation of two major bands at Mr 125,000 and Mr 68,000 was induced by RA in ER+ MCF-7 human breast carcinoma cells. Tretinoin 121-123 estrogen receptor 1 Homo sapiens 127-129 9892191-4 1999 However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h. A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Tretinoin 143-145 estrogen receptor 1 Homo sapiens 162-164 9892191-4 1999 However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h. A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Tretinoin 143-145 estrogen receptor 1 Homo sapiens 231-233 9823320-5 1998 However, stable expression of ER increased retinoid activation of transcription of a retinoic acid (RA) response elements from the low level in MDA-MB-231 to approach the level of MCF-7. Tretinoin 100-102 estrogen receptor 1 Homo sapiens 30-32 11038749-0 1997 [Inhibition of estrogen receptor-positive human breast carcinoma cell growth by retinoic acid]. Tretinoin 80-93 estrogen receptor 1 Homo sapiens 15-32 8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 82-105 estrogen receptor 1 Homo sapiens 14-31 9028736-2 1997 Retinoic acid (RA) inhibition of estrogen receptor (ER)-positive breast carcinoma seems to be mediated through RAR alpha. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 33-50 9028736-2 1997 Retinoic acid (RA) inhibition of estrogen receptor (ER)-positive breast carcinoma seems to be mediated through RAR alpha. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 52-54 9387294-2 1996 It was found that RA could only inhibit the growth of ER-positive but not ER-negative breast cancer cells. Tretinoin 18-20 estrogen receptor 1 Homo sapiens 54-56 9387294-5 1996 When, RAR alpha cDNA was introduced and ixpressed in RA-resistant, ER-negative MDA-MB-231 breast cancer cell line, its growth was strongly inhibited by RA. Tretinoin 6-8 estrogen receptor 1 Homo sapiens 67-69 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 35-52 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 54-56 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 122-124 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 35-52 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 54-56 9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 122-124 8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 82-105 estrogen receptor 1 Homo sapiens 33-35 8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 107-109 estrogen receptor 1 Homo sapiens 14-31 8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 107-109 estrogen receptor 1 Homo sapiens 33-35 1319834-9 1992 Retinoic acid modulation of the estrogen receptor gene mRNA was not responsible for the retinoic acid inhibition of the stimulation of pS2 and TGF-alpha gene expression by estradiol, since estrogen receptor gene expression was increased rather than decreased in the presence of retinoic acid. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 32-49 8300756-0 1993 Estrogen receptor-negative breast cancer cells transfected with the estrogen receptor exhibit increased RAR alpha gene expression and sensitivity to growth inhibition by retinoic acid. Tretinoin 170-183 estrogen receptor 1 Homo sapiens 0-17 8300756-0 1993 Estrogen receptor-negative breast cancer cells transfected with the estrogen receptor exhibit increased RAR alpha gene expression and sensitivity to growth inhibition by retinoic acid. Tretinoin 170-183 estrogen receptor 1 Homo sapiens 68-85 8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 41-54 estrogen receptor 1 Homo sapiens 95-112 8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 41-54 estrogen receptor 1 Homo sapiens 114-116 8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 56-58 estrogen receptor 1 Homo sapiens 95-112 8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 56-58 estrogen receptor 1 Homo sapiens 114-116 8300756-2 1993 The ER-negative cells inherently express lower levels of RAR alpha and retinoic acid response element (RARE)-mediated RA-induced CAT activity. Tretinoin 71-84 estrogen receptor 1 Homo sapiens 4-6 8300756-2 1993 The ER-negative cells inherently express lower levels of RAR alpha and retinoic acid response element (RARE)-mediated RA-induced CAT activity. Tretinoin 57-59 estrogen receptor 1 Homo sapiens 4-6 8300756-3 1993 In this study we report that when ER-negative MDA-MB-231 cells were transfected with the ER gene they not only expressed higher levels of RAR alpha and RARE-mediated RA-induced CAT gene expression, but their growth was not inhibited by RA. Tretinoin 138-140 estrogen receptor 1 Homo sapiens 34-36