PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 59-64 17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 109-114 17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 131-135 17283129-4 2007 Interestingly, we found that miRNA expression levels substantially change in a MYCN-amplified cell line following exposure to retinoic acid, a compound which is well known for causing reductions in MYCN expression and for inducing neuroblastoma cell lines to undergo neuronal differentiation. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 79-83 17283129-4 2007 Interestingly, we found that miRNA expression levels substantially change in a MYCN-amplified cell line following exposure to retinoic acid, a compound which is well known for causing reductions in MYCN expression and for inducing neuroblastoma cell lines to undergo neuronal differentiation. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 198-202 9869047-10 1998 A transcriptional reduction of the N-myc gene by retinoic acid (RA) decreased the motility, which thus resulted in a marked decline of invasiveness in IMR-32 and GOTO. Tretinoin 49-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40 12438307-6 2003 In addition, we provide evidence that E2F proteins are involved in the negative regulation of MYCN by TGF-beta and retinoic acid. Tretinoin 115-128 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-98 11668484-5 2001 Our results show that combined treatment with IFN-gamma and RA or the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA) had synergistic or enhancing effects on morphologic differentiation and neurite outgrowth in 5 of 5 neuroblastoma cell lines, 3 of which expressed very high levels of N-myc mRNA due to N-myc amplification. Tretinoin 60-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 292-297 11668484-5 2001 Our results show that combined treatment with IFN-gamma and RA or the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA) had synergistic or enhancing effects on morphologic differentiation and neurite outgrowth in 5 of 5 neuroblastoma cell lines, 3 of which expressed very high levels of N-myc mRNA due to N-myc amplification. Tretinoin 60-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 310-315 11346880-0 2001 Retinoic acid-induced expression of autotaxin in N-myc-amplified neuroblastoma cells. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 49-54 11107126-3 2000 RESULTS: After 12 exposures to 10 microM ATRA, the two MYCN-amplified cell lines (KCNR 12X RR and LA-N-5 12X RR) showed partial resistance to the cytostatic/differentiation effects of ATRA; complete resistance was seen in LHN 12X RR. Tretinoin 41-45 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 55-59 11107126-3 2000 RESULTS: After 12 exposures to 10 microM ATRA, the two MYCN-amplified cell lines (KCNR 12X RR and LA-N-5 12X RR) showed partial resistance to the cytostatic/differentiation effects of ATRA; complete resistance was seen in LHN 12X RR. Tretinoin 184-188 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 55-59 16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 3-16 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-39 16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 3-16 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 130-134 16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 18-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-39 16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 18-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 130-134 15592517-5 2005 Following treatment with 10 muM RA for 6 days, the MYCN-amplified IGR-N-91 cell lines underwent neuronal differentiation as assessed by reduced MYCN gene expression and neuritic extension. Tretinoin 32-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 51-55 15592517-5 2005 Following treatment with 10 muM RA for 6 days, the MYCN-amplified IGR-N-91 cell lines underwent neuronal differentiation as assessed by reduced MYCN gene expression and neuritic extension. Tretinoin 32-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 144-148 12615055-5 2003 Combination of receptor-specific retinoid agonists for RXR and RAR alpha significantly enhanced the sensitivity of N-myc-amplified neuroblastoma cells to the growth inhibitory effects of aRA. Tretinoin 187-190 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 115-120 12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 64-69 12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 119-124 12700651-2 2003 Retinoic acid (RA) decreases N-myc levels and induces cell cycle arrest in vitro and increases event-free survival in advanced stage NB patients. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 29-34 12700651-2 2003 Retinoic acid (RA) decreases N-myc levels and induces cell cycle arrest in vitro and increases event-free survival in advanced stage NB patients. Tretinoin 15-17 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 29-34 12700651-11 2003 Thus, RA induces both N-myc-dependent and -independent mechanisms to minimize the degradation of p27 and arrest NB cell growth. Tretinoin 6-8 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 22-27 12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 21-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 210-215 12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 210-215 9869047-10 1998 A transcriptional reduction of the N-myc gene by retinoic acid (RA) decreased the motility, which thus resulted in a marked decline of invasiveness in IMR-32 and GOTO. Tretinoin 64-66 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40 9570357-4 1997 Our previous work has shown that RA works synergistically with other agents, such as interferon-gamma (IFN-gamma), to down-regulate N-myc expression and induce differentiation. Tretinoin 33-35 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 132-137 9605760-6 1998 Although GDNF alone induced a rather weak differentiation independent of the disease stages, the enhancement of neurite outgrowth induced by treatment with both GDNF and all-trans-retinoic acid was significantly correlated with younger age (less than 1 year; P = 0.0039), non-stage 4 diseases (P = 0.0023), a single copy of N-myc (P = 0.027), and high levels of TRK-A expression (P = 0.0062). Tretinoin 174-193 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 324-329 8570225-0 1996 Retinoic acid-induced growth arrest and differentiation of neuroblastoma cells are counteracted by N-myc and enhanced by max overexpressions. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 99-104 8570225-1 1996 N-myc expression is negatively regulated by retinoic acid (RA) which induces the growth arrest and differentiation of neuroblastoma (NB) cells. Tretinoin 44-57 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5 8570225-1 1996 N-myc expression is negatively regulated by retinoic acid (RA) which induces the growth arrest and differentiation of neuroblastoma (NB) cells. Tretinoin 59-61 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5 8570225-5 1996 In contrast to N-Myc, Max strongly induced the differentiation by enhancing the effects of RA. Tretinoin 91-93 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 15-20 8519445-4 1995 Retinoic acid decreased N-myc and c-myc and induced neurite outgrowth (a differentiation marker). Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 24-29 7656409-6 1995 These retinoic acid-induced increases in GAP43/B50 and neurite outgrowth, and decreases in N-myc and c-myc, were reversed dose-dependently by alcohol (0-0.5%). Tretinoin 6-19 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 91-96 7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 82-87 7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 162-167 7923112-6 1994 Decreased expression of the N-myc oncogene in neuroblastoma cell lines SH-SY5Y and BE(2)-C, following treatment with retinoic acid, was paralleled by down-regulation of MRP gene expression, contrasting with increased expression of the MDR1 gene. Tretinoin 117-130 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 28-33 1397312-2 1992 Furthermore, plasma membrane redox activity is partially inhibited by retinoic acid in neuroblastoma cells with multiple copies of the N-myc oncogene but not in neuroblastoma cells with only one copy of this gene. Tretinoin 70-83 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 135-140 8108182-4 1993 Using SK-N-SH neuroblastoma cells, we found that RA induced differentiation of SK-N-SH cells as demonstrated by down-regulation of N-myc gene expression, cell-cycle arrest in G1 phase, and phenotypic change. Tretinoin 49-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 131-136 8401251-11 1993 During retinoic acid treatment, N-myc oncogene expression decreases and other genes are deregulated. Tretinoin 7-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 32-37 8331499-7 1993 Treatment of GOTO with 10(-5) mol/L all-trans-retinoic acid (RA) for 72 hours markedly decreased both N-myc expression and invasiveness. Tretinoin 36-59 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 102-107 8331499-7 1993 Treatment of GOTO with 10(-5) mol/L all-trans-retinoic acid (RA) for 72 hours markedly decreased both N-myc expression and invasiveness. Tretinoin 61-63 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 102-107 1565467-6 1992 All tested constructs retaining promoter activity showed decreased activity in parallel with the down-regulation of endogenous N-myc in response to treatment of transfected cells with retinoic acid. Tretinoin 184-197 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 127-132 1419902-4 1992 Although other examples of overlapping, opposite-strand eukaryotic genes exist, N-myc and N-cym are unique in that they appear to be coregulated in tumor cell lines under basal growth conditions and in response to the differentiating agent retinoic acid. Tretinoin 240-253 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 80-85 2013316-0 1991 Expression of protein kinase C-alpha (PKC-alpha) and MYCN mRNAs in human neuroblastoma cells and modulation during morphological differentiation induced by retinoic acid. Tretinoin 156-169 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 53-57 1657899-2 1991 A combination of Bt2cAMP (1 mM) and RA (1 microM) yielded the most significant networks of neurites after 3 to 4 days, this being associated with the reduction of N-myc mRNA levels. Tretinoin 36-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 163-168 2123747-0 1990 Different regulation of mid-size neurofilament and N-myc mRNA expression during neuroblastoma cell differentiation induced by retinoic acid. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 51-56 2068135-0 1991 Patterns of regulation of nuclear proto-oncogenes MYCN and MYB in retinoic acid treated neuroblastoma cells. Tretinoin 66-79 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 50-54 2267130-5 1990 Treatment of the neuroblastoma cell line SMS-KCNR, which contains 75 copies of the N-myc gene, with retinoic acid for ten days resulted in an increase in Op18 phosphorylation. Tretinoin 100-113 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 83-88 35490242-0 2022 The MYCN inhibitor BGA002 restores the retinoic acid response leading to differentiation or apoptosis by the mTOR block in MYCN-amplified neuroblastoma. Tretinoin 39-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 123-127 1697169-1 1990 Expression of myc-box genes can be reduced by Interferon (c-myc in Daudi cells) or Retinoic acid (N-myc in neuroblastoma cells). Tretinoin 83-96 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 98-103 3977910-0 1985 Retinoic acid treatment of human neuroblastoma cells is associated with decreased N-myc expression. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 82-87 2846152-10 1988 The Kelly cell line with amplified N-myc genome, which correlates with clinical progression of neuroblastoma, was also sensitive to RA plus herb-A. Tretinoin 132-134 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40 2917804-4 1989 Decreased N-myc expression and increased c-src expression were observed during neuronal differentiation by retinoic acid, polyprenoic acid (E5166) and dibutyryl cyclic AMP, whereas the expression of N-myc and c-src genes was considerably reduced during schwannian differentiation by bromodeoxyuridine, demonstrating that the expression of N-myc and c-src genes was regulated independently in the bipolar differentiation processes of NB cells. Tretinoin 107-120 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 10-15 2480694-2 1989 Expression of N-myc gene product was reduced in neuroblastoma cell line SK-N-DZ differentiated by retinoic acid as compared with untreated cells. Tretinoin 98-111 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 14-19 3325885-6 1987 In contrast, when the cells were exposed to retinoic acid, which results in a maturation along an alternative pathway, the inhibition of N-myc and c-myc expression was similar. Tretinoin 44-57 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 137-142 3977910-2 1985 We report here that N-myc mRNA content is markedly decreased in cells of a neuroblastoma cell line (LA-N-5) following differentiation induced with retinoic acid. Tretinoin 147-160 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 20-25 3977910-3 1985 Exposure of the cells to retinoic acid induced morphologic changes consistent with neuronal differentiation, and led to a 75% decrease in expression of N-myc mRNA. Tretinoin 25-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 152-157 32240058-0 2020 MYCN Silencing by RNA Interference Induces Neurogenesis and Suppresses Proliferation in Models of Neuroblastoma with Resistance to Retinoic Acid. Tretinoin 131-144 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-4 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 25-29 32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 25-29 3855502-0 1985 Decreased expression of N-myc precedes retinoic acid-induced morphological differentiation of human neuroblastoma. Tretinoin 39-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 24-29 32240058-9 2020 Our result suggests that gene therapy using RNAi targeting MYCN can be a novel therapy toward MYCN-amplified NB that have complete or partial resistance toward RA. Tretinoin 160-162 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 59-63 32240058-9 2020 Our result suggests that gene therapy using RNAi targeting MYCN can be a novel therapy toward MYCN-amplified NB that have complete or partial resistance toward RA. Tretinoin 160-162 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-98 32006898-0 2020 Decitabine and all-trans retinoic acid synergistically exhibit cytotoxicity against elderly AML patients via miR-34a/MYCN axis. Tretinoin 15-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 117-121 31903789-5 2020 Here, we demonstrate that in cultured neuroblastoma tumour cells, RAMBAs enhance RA action as seen by morphological differentiation, AKT signalling and suppression of MYCN protein. Tretinoin 66-68 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171 32006898-6 2020 Meanwhile, we found DAC and ATRA inhibited DNMT1, activated miR-34a via promoter hypomethylation, down-regulated its target MYCN and thus exerted a synergistic antineoplastic effect. Tretinoin 28-32 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 124-128 32006898-7 2020 In conclusion, DAC plus ATRA regimen might be effective and well-tolerated for elderly patients partially through modulating miR-34a/MYCN axis. Tretinoin 24-28 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 133-137 32064173-0 2020 Erratum: Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 40-63 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 134-138 32087738-7 2020 We examined the effect of retinoic acid, the differentiation agent used in neuroblastoma therapy, on miR-506-3p, PLAGL2 and MYCN expressions by quantitative PCR and Western blots. Tretinoin 26-39 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 124-128 32087738-14 2020 Furthermore, we found that retinoic acid increased expression of miR-506-3p and repressed expression of MYCN and PLAGL2. Tretinoin 27-40 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 104-108 32087738-15 2020 CONCLUSIONS: Our findings altogether suggest that the interplay network formed by PLAGL2, MYCN and miR-506-3p is an important mechanism in regulating neuroblastoma cell fate, determining neuroblastoma prognosis, and mediating the therapeutic function of retinoic acid. Tretinoin 254-267 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 90-94 31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 44-48 31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171 31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 44-48 31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171 31262872-3 2019 We recently found that combination of all-trans retinoic acid (ATRA) with the beta1-integrin-activating peptide TNIIIA2 attenuated cancer-associated properties of neuroblastoma cells through N-Myc degradation. Tretinoin 38-61 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 191-196 31262872-3 2019 We recently found that combination of all-trans retinoic acid (ATRA) with the beta1-integrin-activating peptide TNIIIA2 attenuated cancer-associated properties of neuroblastoma cells through N-Myc degradation. Tretinoin 63-67 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 191-196 28927789-2 2017 The human high-risk neuroblastoma cell line, SK-N-AS (non-amplified N-myc) is derived from stromal cells and it is resistant to treatment with retinoic acid (1, RA), which is a chemotherapeutic agent used to induce neuronal cellular differentiation of neuroblastomas. Tretinoin 143-156 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 68-73 30906641-0 2019 Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 41-54 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 67-72 30906641-0 2019 Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 41-54 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 125-129 30906641-7 2019 However, the clinical outcome has not been sufficient with the use of retinoids, including all-trans retinoic acid (ATRA), mainly because of the inhibition of differentiation caused by N-Myc. Tretinoin 91-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 185-190 30906641-7 2019 However, the clinical outcome has not been sufficient with the use of retinoids, including all-trans retinoic acid (ATRA), mainly because of the inhibition of differentiation caused by N-Myc. Tretinoin 116-120 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 185-190 30906641-8 2019 In the present study, we succeeded in synergistically accelerating the ATRA-induced neuronal differentiation of MYCN-amplified neuroblastoma cells by combining a peptide derived from tenascin-C, termed TNIIIA2, which has a potent ability to activate beta1-integrins. Tretinoin 71-75 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 112-116 30906641-9 2019 Accelerated differentiation was caused by a decrease in N-Myc protein level in neuroblastoma cells after the combined treatment of TNIIIA2 with ATRA. Tretinoin 144-148 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 56-61 30906641-10 2019 That is, combination treatment using ATRA with TNIIIA2 induced proteasomal degradation in the N-Myc oncoprotein of neuroblastoma cells with MYCN gene amplification, and this caused acceleration of neuronal differentiation and attenuation of malignant properties. Tretinoin 37-41 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-99 30906641-10 2019 That is, combination treatment using ATRA with TNIIIA2 induced proteasomal degradation in the N-Myc oncoprotein of neuroblastoma cells with MYCN gene amplification, and this caused acceleration of neuronal differentiation and attenuation of malignant properties. Tretinoin 37-41 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 140-144 29301505-5 2018 METHODS: As a proof of principle, differentiation upon ATRA treatment of two MYCN-amplified neuroblastoma cell lines, IMR32 and BE2C, was measured both in cell cultures and in tumours formed on the chick chorioallantoic membrane (CAM). Tretinoin 55-59 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 77-81 28187790-0 2017 Retinoic acid and TGF-beta signalling cooperate to overcome MYCN-induced retinoid resistance. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 60-64 28187790-5 2017 We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 11-15 28187790-5 2017 We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 39-43 28187790-11 2017 Co-targeting of the retinoic acid and TGF-beta pathways, through RA and kartogenin (KGN; a TGF-beta signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Tretinoin 20-33 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 194-198 27531891-6 2016 Wnt and retinoic acid co-treatments synergise, representing a promising combination treatment for MYCN-amplified neuroblastoma. Tretinoin 8-21 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 98-102 25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 42-46 25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 157-161 23565812-3 2013 All-trans-retinoic acid (ATRA) causes some neuroblastoma (NB) cell lines to undergo differentiation and leads to a significant decrease in the oncogenic transcription factor MYCN. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 174-178 23565812-3 2013 All-trans-retinoic acid (ATRA) causes some neuroblastoma (NB) cell lines to undergo differentiation and leads to a significant decrease in the oncogenic transcription factor MYCN. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 174-178 17554788-0 2008 Retinoic acid induced downregulation of MYCN is not mediated through changes in Sp1/Sp3. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 40-44 19550295-0 2010 Effect of cytotoxic agents and retinoic acid on Myc-N protein expression in neuroblastoma. Tretinoin 31-44 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 48-53 19550295-13 2010 Myc-N expression was negative in retinoic acid combined with vincristine group. Tretinoin 33-46 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5 18949372-3 2008 Retinoic acid (RA), a molecule able to induce differentiation and to decrease MYCN expression, is used in the therapy of neuroblastomas. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 78-82 18949372-3 2008 Retinoic acid (RA), a molecule able to induce differentiation and to decrease MYCN expression, is used in the therapy of neuroblastomas. Tretinoin 15-17 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 78-82 21908575-7 2011 RESULTS: The expression of NLRR3 mRNA was upregulated during differentiation of NBL cells induced by retinoic acid, accompanied with reduced expression of MYCN, suggesting that NLRR3 expression was inversely correlated with MYCN in differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 224-228 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 61-65 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 61-65 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92 19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92 17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 110-114 17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 314-318