PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27400858-8 2017 A complementary ability to enhance TPA-induced AP-1 transcription was observed, even at concentrations insufficient to activate the ERalpha, suggesting a partly independent mechanism. Tetradecanoylphorbol Acetate 35-38 estrogen receptor 1 Homo sapiens 132-139 25728938-9 2015 Notably, loss of ERalpha promoted breast cancer cell migration and invasion by inducing changes in the expression levels of certain matrix macromolecules (especially uPA, tPA, PAI-1) through the EGFR-ERK signaling pathway. Tetradecanoylphorbol Acetate 171-174 estrogen receptor 1 Homo sapiens 17-24 28035371-4 2017 In ER-positive MCF-7 cells, arctigenin efficiently inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell migration and invasion. Tetradecanoylphorbol Acetate 99-102 estrogen receptor 1 Homo sapiens 3-5 16651411-9 2006 In the presence of TPA, whereas ERalpha was not bound to the promoter, a strong association of acetylated and/or phospho-H3, MSK1, and c-Jun was observed. Tetradecanoylphorbol Acetate 19-22 estrogen receptor 1 Homo sapiens 32-39 18668201-5 2008 ERalpha and ERbeta interact with NFAT3 independently of the NFAT agonists phorbol myristate acetate (PMA) and ionomycin, and ERalpha is recruited to an NFAT3 target gene promoter. Tetradecanoylphorbol Acetate 101-104 estrogen receptor 1 Homo sapiens 0-7 15282324-3 2004 We report here that CCND1 promoter activation by estrogens in human breast cancer cells is mediated by recruitment of a c-Jun/c-Fos/estrogen receptor alpha complex to the tetradecanoyl phorbol acetate-responsive element of the gene, together with Oct-1 to a site immediately adjacent. Tetradecanoylphorbol Acetate 171-200 estrogen receptor 1 Homo sapiens 132-155 15824731-6 2005 Furthermore, activation of PKCdelta by TPA resulted in activation and nuclear translocation of ERalpha and in an increase of ER-dependent reporter gene expression. Tetradecanoylphorbol Acetate 39-42 estrogen receptor 1 Homo sapiens 95-102 15824731-7 2005 Transfection and expression of the regulatory domain RDdelta of PKCdelta, which is inhibitory to PKCdelta, inhibited the TPA-induced ERalpha activation and translocation. Tetradecanoylphorbol Acetate 121-124 estrogen receptor 1 Homo sapiens 133-140 11840342-8 2002 TPA causes positive regulation of Cyr61 expression in ER-positive MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 estrogen receptor 1 Homo sapiens 54-56 9706865-4 1998 To characterize these relationships further, we examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), which downregulates ERalpha, and the high-affinity AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on the expression of AhR, ERalpha, CYP1A1, and CYP1B1 in MCF-7 human breast cancer cells. Tetradecanoylphorbol Acetate 110-113 estrogen receptor 1 Homo sapiens 136-143 11061546-15 2000 In agreement with the semiquantitative RT-PCR results, Western blot analysis detected a decrease in ERalpha and ERbeta proteins levels in hGLCs after treatment with hCG (10 IU/mL), GnRH (0.1 micromol/L), 8-bromo-cAMP (1 mmol/L), forskolin (10 micromol/L), or phorbol 12-myristate 13 acetate (10 micromol/L). Tetradecanoylphorbol Acetate 259-290 estrogen receptor 1 Homo sapiens 100-107 9877207-6 1998 ERalpha/E2 also induced a two-fold potentiation of TPA-mediated expression of beta-galactosidase under the control of TREs in HeLa cells but not in HEK-293 cells. Tetradecanoylphorbol Acetate 51-54 estrogen receptor 1 Homo sapiens 0-7 9706865-5 1998 Treatment with TPA, which suppressed ERalpha mRNA levels, caused a greater than fourfold elevation of AhR mRNA and protein levels, whereas treatment with TCDD caused a decrease in AhR protein but no change in ERalpha or AhR mRNA levels. Tetradecanoylphorbol Acetate 15-18 estrogen receptor 1 Homo sapiens 37-44 9706865-6 1998 In MCF-7 cells treated with TPA prior to treatment with TCDD, the AhR mRNA level was elevated, the ERalpha mRNA level remained suppressed, and the ratio of CYP1B1 to CYP1A1 mRNA was increased compared with treatment with TCDD alone. Tetradecanoylphorbol Acetate 28-31 estrogen receptor 1 Homo sapiens 99-106 8655628-3 1996 Comparative studies were conducted with E2 and 12-O-tetradecanoylphorbol-13-acetate (TPA), as both compounds are known to suppress ER expression. Tetradecanoylphorbol Acetate 47-83 estrogen receptor 1 Homo sapiens 131-133 9065603-5 1997 Incubation with phorbol-12-myristate-13-acetate led to a significant increase (p < 0.005) of LDL-R mRNA in ER+ cells, whereas in ER- cells LDL-R mRNA levels remained merely unchanged. Tetradecanoylphorbol Acetate 16-47 estrogen receptor 1 Homo sapiens 110-112 8655628-0 1996 Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin, 12-O-tetradecanoylphorbol-13-acetate and 17 beta-estradiol on estrogen receptor regulation in MCF-7 human breast cancer cells. Tetradecanoylphorbol Acetate 48-84 estrogen receptor 1 Homo sapiens 110-127 8655628-3 1996 Comparative studies were conducted with E2 and 12-O-tetradecanoylphorbol-13-acetate (TPA), as both compounds are known to suppress ER expression. Tetradecanoylphorbol Acetate 85-88 estrogen receptor 1 Homo sapiens 131-133 8655628-4 1996 Our results indicate that 1 nM E2 and 100 nM TPA both suppress ER mRNA levels as early as 4 h after exposure and to 33.6% and 16.5% of control levels, respectively, after 72 h. In contrast, no significant effect on ER mRNA levels was attributed to exposure to 10 nM TCDD. Tetradecanoylphorbol Acetate 45-48 estrogen receptor 1 Homo sapiens 63-65 8655628-4 1996 Our results indicate that 1 nM E2 and 100 nM TPA both suppress ER mRNA levels as early as 4 h after exposure and to 33.6% and 16.5% of control levels, respectively, after 72 h. In contrast, no significant effect on ER mRNA levels was attributed to exposure to 10 nM TCDD. Tetradecanoylphorbol Acetate 45-48 estrogen receptor 1 Homo sapiens 215-217 8655628-5 1996 A greater than 50% reduction in positive staining was observed by ER-ICA after 72 h exposure to 1 nM E2 and to 100 nM TPA, while only an 11% reduction in positive staining was observed with 10 nM TCDD. Tetradecanoylphorbol Acetate 118-121 estrogen receptor 1 Homo sapiens 66-68 8655628-8 1996 In conclusion, while TPA and E2 effectively down-regulate ER expression, TCDD, under antiestrogenic conditions, has little if any effect on total ER levels in MCF-7 cells, and thus ER modulation is probably not necessary for the suppression of estrogenic activity in MCF-7 cells by TCDD. Tetradecanoylphorbol Acetate 21-24 estrogen receptor 1 Homo sapiens 58-60 8378087-2 1993 The chimaeric Fos-ER proteins showed estrogen-inducible activation of TRE (TPA-responsive element)-directed transcription and hormone-dependent transformation of fibroblasts. Tetradecanoylphorbol Acetate 75-78 estrogen receptor 1 Homo sapiens 18-20 7559663-0 1995 Effects of 12-O-tetradecanoylphorbol-13-acetate on estrogen receptor activity in MCF-7 cells. Tetradecanoylphorbol Acetate 11-47 estrogen receptor 1 Homo sapiens 51-68 7559663-1 1995 The effects of long term treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) on estrogen receptor (ER) expression in the human breast cancer cell line, MCF-7, were studied. Tetradecanoylphorbol Acetate 40-76 estrogen receptor 1 Homo sapiens 86-103 7559663-1 1995 The effects of long term treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) on estrogen receptor (ER) expression in the human breast cancer cell line, MCF-7, were studied. Tetradecanoylphorbol Acetate 40-76 estrogen receptor 1 Homo sapiens 105-107 7559663-1 1995 The effects of long term treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) on estrogen receptor (ER) expression in the human breast cancer cell line, MCF-7, were studied. Tetradecanoylphorbol Acetate 78-81 estrogen receptor 1 Homo sapiens 86-103 7559663-1 1995 The effects of long term treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) on estrogen receptor (ER) expression in the human breast cancer cell line, MCF-7, were studied. Tetradecanoylphorbol Acetate 78-81 estrogen receptor 1 Homo sapiens 105-107 7559663-3 1995 Treatment of cells with 100 nM TPA resulted in an 80% decrease in the level of ER protein and a parallel decrease in ER mRNA and binding capacity. Tetradecanoylphorbol Acetate 31-34 estrogen receptor 1 Homo sapiens 79-81 7559663-3 1995 Treatment of cells with 100 nM TPA resulted in an 80% decrease in the level of ER protein and a parallel decrease in ER mRNA and binding capacity. Tetradecanoylphorbol Acetate 31-34 estrogen receptor 1 Homo sapiens 117-119 7559663-4 1995 Following removal of TPA from the medium, the level of ER protein and mRNA returned to control values; however, the receptor failed to bind estradiol. Tetradecanoylphorbol Acetate 21-24 estrogen receptor 1 Homo sapiens 55-57 7559663-6 1995 In addition, TPA treatment blocked transcription from an estrogen response element in transient transfection assays and inhibited ER binding to its response element in a DNA mobility shift assay. Tetradecanoylphorbol Acetate 13-16 estrogen receptor 1 Homo sapiens 130-132 7559663-9 1995 Mixing experiments suggest that TPA induces/activates a factor which interacts with the ER to block binding of estradiol. Tetradecanoylphorbol Acetate 32-35 estrogen receptor 1 Homo sapiens 88-90 7559663-10 1995 The effects of TPA on ER levels and binding capacity were concentration-dependent. Tetradecanoylphorbol Acetate 15-18 estrogen receptor 1 Homo sapiens 22-24 7867590-5 1995 Secondly, in prolonged (4-day) treatments of MTLN (ER-positive) cells, low antiestrogen concentrations (nanomolar) decreased the basal AP-1 response by about 2 and increased the 12-O-tetradecanoyl-phorbol-13-acetate-stimulated AP-1 response by about 3-4. Tetradecanoylphorbol Acetate 178-215 estrogen receptor 1 Homo sapiens 51-53 8308015-5 1994 Tryptic phosphopeptide analysis of ER, using a two-dimensional peptide mapping procedure, revealed similar patterns for ER in cells treated with estradiol, antiestrogens or TPA; with CT+IBMX treatment, the same phosphopeptides were seen, but the relative phosphorylation of the different ER phosphotryptic peptides differed. Tetradecanoylphorbol Acetate 173-176 estrogen receptor 1 Homo sapiens 120-122 8308015-5 1994 Tryptic phosphopeptide analysis of ER, using a two-dimensional peptide mapping procedure, revealed similar patterns for ER in cells treated with estradiol, antiestrogens or TPA; with CT+IBMX treatment, the same phosphopeptides were seen, but the relative phosphorylation of the different ER phosphotryptic peptides differed. Tetradecanoylphorbol Acetate 173-176 estrogen receptor 1 Homo sapiens 120-122 1917923-0 1991 Post-transcriptional destabilization of estrogen receptor mRNA in MCF-7 cells by 12-O-tetradecanoylphorbol-13-acetate. Tetradecanoylphorbol Acetate 81-117 estrogen receptor 1 Homo sapiens 40-57 1382961-2 1992 Treatment of MCF-7 cells, a human mammary adenocarcinoma cell line, with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (10-7 M) was associated with a time-dependent reduction in the level of estrogen receptor (ER) mRNA (half-life approximately 3 h). Tetradecanoylphorbol Acetate 91-127 estrogen receptor 1 Homo sapiens 206-223 1382961-2 1992 Treatment of MCF-7 cells, a human mammary adenocarcinoma cell line, with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (10-7 M) was associated with a time-dependent reduction in the level of estrogen receptor (ER) mRNA (half-life approximately 3 h). Tetradecanoylphorbol Acetate 91-127 estrogen receptor 1 Homo sapiens 225-227 1382961-2 1992 Treatment of MCF-7 cells, a human mammary adenocarcinoma cell line, with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (10-7 M) was associated with a time-dependent reduction in the level of estrogen receptor (ER) mRNA (half-life approximately 3 h). Tetradecanoylphorbol Acetate 129-132 estrogen receptor 1 Homo sapiens 206-223 1382961-2 1992 Treatment of MCF-7 cells, a human mammary adenocarcinoma cell line, with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (10-7 M) was associated with a time-dependent reduction in the level of estrogen receptor (ER) mRNA (half-life approximately 3 h). Tetradecanoylphorbol Acetate 129-132 estrogen receptor 1 Homo sapiens 225-227 1382961-4 1992 Furthermore, the TPA-dependent down-regulation of ER mRNA was abolished by actinomycin D. Tetradecanoylphorbol Acetate 17-20 estrogen receptor 1 Homo sapiens 50-52 1382961-7 1992 Our studies show that degradation of ER mRNA by TPA in MCF-7 cells is dependent on ongoing RNA synthesis but not on protein synthesis. Tetradecanoylphorbol Acetate 48-51 estrogen receptor 1 Homo sapiens 37-39 1382961-8 1992 This indicates that an RNA molecule with rapid turnover, which does not require translation, might be involved in the TPA-dependent ER mRNA decay. Tetradecanoylphorbol Acetate 118-121 estrogen receptor 1 Homo sapiens 132-134 1917923-1 1991 The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of the estrogen receptor (ER) was investigated in this study. Tetradecanoylphorbol Acetate 14-50 estrogen receptor 1 Homo sapiens 82-99 1917923-1 1991 The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of the estrogen receptor (ER) was investigated in this study. Tetradecanoylphorbol Acetate 14-50 estrogen receptor 1 Homo sapiens 101-103 1917923-1 1991 The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of the estrogen receptor (ER) was investigated in this study. Tetradecanoylphorbol Acetate 52-55 estrogen receptor 1 Homo sapiens 82-99 1917923-1 1991 The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of the estrogen receptor (ER) was investigated in this study. Tetradecanoylphorbol Acetate 52-55 estrogen receptor 1 Homo sapiens 101-103 1917923-3 1991 By 24 h the receptor protein declined by about 80% from a level of approximately 236 fmol of ER/mg of protein in control cells to 50 fmol of ER/mg of protein in cells treated with TPA. Tetradecanoylphorbol Acetate 180-183 estrogen receptor 1 Homo sapiens 141-143 1917923-5 1991 After removal of TPA, the level of ER returned to control values. Tetradecanoylphorbol Acetate 17-20 estrogen receptor 1 Homo sapiens 35-37 1917923-7 1991 The effects of TPA on ER expression appear to be mediated by activation of protein kinase C as H-7, an inhibitor of protein kinase C, blocks these effects. Tetradecanoylphorbol Acetate 15-18 estrogen receptor 1 Homo sapiens 22-24 1917923-8 1991 In addition to the effect on ER protein, TPA treatment also resulted in a decrease in the steady-state level of ER mRNA as determined by a RNase protection assay. Tetradecanoylphorbol Acetate 41-44 estrogen receptor 1 Homo sapiens 29-31 1917923-8 1991 In addition to the effect on ER protein, TPA treatment also resulted in a decrease in the steady-state level of ER mRNA as determined by a RNase protection assay. Tetradecanoylphorbol Acetate 41-44 estrogen receptor 1 Homo sapiens 112-114 1917923-11 1991 A half-life study demonstrated that TPA decreased ER mRNA half-life by a factor of 6 from approximately 4 h in control cells to 40 min in TPA-treated cells. Tetradecanoylphorbol Acetate 36-39 estrogen receptor 1 Homo sapiens 50-52 1917923-11 1991 A half-life study demonstrated that TPA decreased ER mRNA half-life by a factor of 6 from approximately 4 h in control cells to 40 min in TPA-treated cells. Tetradecanoylphorbol Acetate 138-141 estrogen receptor 1 Homo sapiens 50-52 2751660-3 1989 Exposure to 10 nM TPA resulted in a time-dependent increase in EGF-R mRNA, first apparent at 3 h and maximal between 9 and 24 h. There was a concomitant fall in ER mRNA with a maximum decline to 15-20% of control between 12 and 24 h. Although EGF-R mRNA levels declined between 24 and 72 h, both EGF-R mRNA and EGF-R binding remained above control levels and this was accompanied by a sustained depression of ER mRNA. Tetradecanoylphorbol Acetate 18-21 estrogen receptor 1 Homo sapiens 161-163 2055193-1 1991 Treatment of MCF-7 cells, a human mammary carcinoma cell line, with phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TPA)] or calcium ionophore (A23187) was associated with striking effects on levels of estrogen receptor (ER) mRNA, specific binding of 17 beta-[3H]estradiol [( 3H]E2), and immunoreactive ER. Tetradecanoylphorbol Acetate 83-119 estrogen receptor 1 Homo sapiens 207-224 2055193-1 1991 Treatment of MCF-7 cells, a human mammary carcinoma cell line, with phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TPA)] or calcium ionophore (A23187) was associated with striking effects on levels of estrogen receptor (ER) mRNA, specific binding of 17 beta-[3H]estradiol [( 3H]E2), and immunoreactive ER. Tetradecanoylphorbol Acetate 83-119 estrogen receptor 1 Homo sapiens 226-228 2055193-1 1991 Treatment of MCF-7 cells, a human mammary carcinoma cell line, with phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TPA)] or calcium ionophore (A23187) was associated with striking effects on levels of estrogen receptor (ER) mRNA, specific binding of 17 beta-[3H]estradiol [( 3H]E2), and immunoreactive ER. Tetradecanoylphorbol Acetate 83-119 estrogen receptor 1 Homo sapiens 308-310 2379149-8 1990 Saturation analysis revealed marked differences between the effects of TPA on EGF binding in ER+ and ER- cell lines. Tetradecanoylphorbol Acetate 71-74 estrogen receptor 1 Homo sapiens 93-95 2379149-8 1990 Saturation analysis revealed marked differences between the effects of TPA on EGF binding in ER+ and ER- cell lines. Tetradecanoylphorbol Acetate 71-74 estrogen receptor 1 Homo sapiens 101-103 2379149-9 1990 In ER+ cell lines, 2-h treatment with 10 nM TPA resulted in a marked reduction in the number of high affinity EGF-R sites and a significant decrease in binding affinity. Tetradecanoylphorbol Acetate 44-47 estrogen receptor 1 Homo sapiens 3-5 2379149-13 1990 These data demonstrate differential relationships between TPA-induced changes in growth and EGF-R binding in ER+ and ER- breast cancer cells, thus supporting the view that growth regulatory pathways are markedly different in these two subtypes of human breast cancer. Tetradecanoylphorbol Acetate 58-61 estrogen receptor 1 Homo sapiens 109-111 2379149-13 1990 These data demonstrate differential relationships between TPA-induced changes in growth and EGF-R binding in ER+ and ER- breast cancer cells, thus supporting the view that growth regulatory pathways are markedly different in these two subtypes of human breast cancer. Tetradecanoylphorbol Acetate 58-61 estrogen receptor 1 Homo sapiens 117-119 2055193-2 1991 TPA (10(-7) M) caused a time-dependent reduction of ER mRNA which was below the level of detection after 9 h. Similar effects of TPA appeared at levels of specific binding of [3H]E2 as well as immunoreactive ER. Tetradecanoylphorbol Acetate 0-3 estrogen receptor 1 Homo sapiens 52-54 2055193-2 1991 TPA (10(-7) M) caused a time-dependent reduction of ER mRNA which was below the level of detection after 9 h. Similar effects of TPA appeared at levels of specific binding of [3H]E2 as well as immunoreactive ER. Tetradecanoylphorbol Acetate 0-3 estrogen receptor 1 Homo sapiens 208-210 2055193-2 1991 TPA (10(-7) M) caused a time-dependent reduction of ER mRNA which was below the level of detection after 9 h. Similar effects of TPA appeared at levels of specific binding of [3H]E2 as well as immunoreactive ER. Tetradecanoylphorbol Acetate 129-132 estrogen receptor 1 Homo sapiens 52-54 2055193-2 1991 TPA (10(-7) M) caused a time-dependent reduction of ER mRNA which was below the level of detection after 9 h. Similar effects of TPA appeared at levels of specific binding of [3H]E2 as well as immunoreactive ER. Tetradecanoylphorbol Acetate 129-132 estrogen receptor 1 Homo sapiens 208-210 2055193-4 1991 Incubation of MCF-7 cells with increasing concentrations of TPA (10(-11)-10(-7) M) was associated with biphasic effects on ER mRNA and proteins. Tetradecanoylphorbol Acetate 60-63 estrogen receptor 1 Homo sapiens 123-125 2751660-3 1989 Exposure to 10 nM TPA resulted in a time-dependent increase in EGF-R mRNA, first apparent at 3 h and maximal between 9 and 24 h. There was a concomitant fall in ER mRNA with a maximum decline to 15-20% of control between 12 and 24 h. Although EGF-R mRNA levels declined between 24 and 72 h, both EGF-R mRNA and EGF-R binding remained above control levels and this was accompanied by a sustained depression of ER mRNA. Tetradecanoylphorbol Acetate 18-21 estrogen receptor 1 Homo sapiens 409-411