PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 20-23 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-43 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 90-93 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 95-108 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 RELA proto-oncogene, NF-kB subunit Homo sapiens 110-114 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-120 32780889-11 2020 CUDC-907 suppressed Akt, NF-kappaB and AP-1 by downregulating phosphorylated and/or total Akt, IKKalpha/beta, RelA, JunB and JunD. CUDC-907 0-8 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-129 32200503-7 2020 Knockdown of DR5 abrogated apoptosis induced by the combination of CUDC-907 and TRAIL in breast cancer cells. CUDC-907 67-75 TNF receptor superfamily member 10b Homo sapiens 13-16 32200503-8 2020 CUDC-907 increased the phosphorylation of JNK and p38 MAPK. CUDC-907 0-8 mitogen-activated protein kinase 8 Homo sapiens 42-45 32200503-8 2020 CUDC-907 increased the phosphorylation of JNK and p38 MAPK. CUDC-907 0-8 mitogen-activated protein kinase 14 Homo sapiens 50-53 32200503-0 2020 CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells. CUDC-907 0-8 TNF superfamily member 10 Homo sapiens 18-23 32200503-9 2020 JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5. CUDC-907 38-46 mitogen-activated protein kinase 8 Homo sapiens 0-3 32200503-0 2020 CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells. CUDC-907 0-8 TNF receptor superfamily member 10b Homo sapiens 66-69 32200503-9 2020 JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5. CUDC-907 38-46 TNF receptor superfamily member 10b Homo sapiens 71-74 32200503-10 2020 In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation. CUDC-907 12-20 TNF superfamily member 10 Homo sapiens 91-96 32200503-1 2020 CUDC-907 is a novel dual-acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC). CUDC-907 0-8 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 45-70 32200503-5 2020 The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells. CUDC-907 26-34 TNF superfamily member 10 Homo sapiens 96-101 32200503-10 2020 In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation. CUDC-907 12-20 TNF receptor superfamily member 10b Homo sapiens 124-127 30819918-5 2019 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc. CUDC-907 0-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 70-75 32200503-5 2020 The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells. CUDC-907 26-34 poly(ADP-ribose) polymerase 1 Homo sapiens 162-208 32200503-5 2020 The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells. CUDC-907 26-34 poly(ADP-ribose) polymerase 1 Homo sapiens 210-214 32200503-6 2020 CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. CUDC-907 0-8 TNF receptor superfamily member 10b Homo sapiens 33-49 32200503-6 2020 CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. CUDC-907 0-8 TNF receptor superfamily member 10b Homo sapiens 51-54 32200503-6 2020 CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. CUDC-907 0-8 X-linked inhibitor of apoptosis Homo sapiens 104-108 32200503-6 2020 CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. CUDC-907 0-8 BCL2 apoptosis regulator Homo sapiens 110-115 32200503-6 2020 CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. CUDC-907 0-8 BCL2 like 1 Homo sapiens 120-126 33069237-0 2020 The dual HDAC-PI3K inhibitor CUDC-907 displays single-agent activity and synergizes with PARP inhibitor olaparib in small cell lung cancer. CUDC-907 29-37 poly(ADP-ribose) polymerase 1 Homo sapiens 89-93 33069237-7 2020 RESULTS: CUDC-907 treatment downregulated MYC paralogs and FoxM1, induced G1 cell-cycle arrest, and impaired DNA double-strand break (DSB) repair capacity in SCLC cells, which produced a potent antiproliferative effect. CUDC-907 9-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-45 33069237-7 2020 RESULTS: CUDC-907 treatment downregulated MYC paralogs and FoxM1, induced G1 cell-cycle arrest, and impaired DNA double-strand break (DSB) repair capacity in SCLC cells, which produced a potent antiproliferative effect. CUDC-907 9-17 forkhead box M1 Homo sapiens 59-64 33069237-8 2020 Furthermore, we showed that CUDC-907 treatment enhanced the therapeutic efficacy of PARP inhibitor olaparib in SCLC cellular models and a PDX model. CUDC-907 28-36 poly(ADP-ribose) polymerase 1 Homo sapiens 84-88 33069237-9 2020 Mechanistic investigations demonstrated that CUDC-907 synergized with olaparib through the blockade of DSB repair pathways and downregulation of MYC paralogs and FoxM1. CUDC-907 45-53 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-148 33069237-9 2020 Mechanistic investigations demonstrated that CUDC-907 synergized with olaparib through the blockade of DSB repair pathways and downregulation of MYC paralogs and FoxM1. CUDC-907 45-53 forkhead box M1 Homo sapiens 162-167 33069237-10 2020 CONCLUSIONS: Our study uncovers that dual PI3K and HDAC inhibition by CUDC-907 exerts significant single-agent activity and strong synergistic effects with PARP inhibitor olaparib in SCLC, which thus provides a rational combination treatment strategy for SCLC clinical investigation. CUDC-907 70-78 poly(ADP-ribose) polymerase 1 Homo sapiens 156-160 32943605-8 2020 CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones. CUDC-907 0-8 SMAD family member 2 Mus musculus 136-143 32943605-10 2020 Overall, these data suggest that dual inhibition of HDAC and the tyrosine kinase signaling pathways with CUDC-907 is a promising treatment strategy for TGFbeta1-induced lung and tumor fibrosis. CUDC-907 105-113 transforming growth factor, beta 1 Mus musculus 152-160 32459381-6 2020 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc. CUDC-907 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 54-59 32459381-6 2020 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc. CUDC-907 0-8 BCL2 like 1 Homo sapiens 61-67 32459381-6 2020 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc. CUDC-907 0-8 BCL2 like 11 Homo sapiens 69-72 32459381-6 2020 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc. CUDC-907 0-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-82 32459381-7 2020 Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis. CUDC-907 69-77 WEE1 G2 checkpoint kinase Homo sapiens 28-32 32459381-7 2020 Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis. CUDC-907 69-77 checkpoint kinase 1 Homo sapiens 34-38 32459381-7 2020 Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis. CUDC-907 69-77 ribonucleotide reductase catalytic subunit M1 Homo sapiens 40-44 32459381-7 2020 Further, down-regulation of Wee1, CHK1, RRM1 and RRM2 contributed to CUDC-907-induced DNA damage and apoptosis. CUDC-907 69-77 ribonucleotide reductase regulatory subunit M2 Homo sapiens 49-53 31901955-3 2020 Furthermore, CUDC-907 is an oral inhibitor of class I phosphoinositide 3-kinase (PI3K) as well as class I and II histone deacetylase (HDAC) enzymes. CUDC-907 13-21 histone deacetylase 9 Homo sapiens 113-132 31901955-3 2020 Furthermore, CUDC-907 is an oral inhibitor of class I phosphoinositide 3-kinase (PI3K) as well as class I and II histone deacetylase (HDAC) enzymes. CUDC-907 13-21 histone deacetylase 9 Homo sapiens 134-138 31901955-4 2020 METHODS: In this study, we evaluated the effect of combination therapy of CUDC-907 and ABL TKIs, using BCR-ABL-positive cell lines and primary samples. CUDC-907 74-82 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 103-110 31901955-10 2020 CONCLUSION: Taken together, our results indicate that administration of CUDC-907, a dual PI3K and HDAC inhibitor, may be an effective strategy against ABL TKI-resistant cells, including cells harboring the T315I mutation. CUDC-907 72-80 histone deacetylase 9 Homo sapiens 98-102 31901955-10 2020 CONCLUSION: Taken together, our results indicate that administration of CUDC-907, a dual PI3K and HDAC inhibitor, may be an effective strategy against ABL TKI-resistant cells, including cells harboring the T315I mutation. CUDC-907 72-80 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 151-154 31901955-11 2020 Moreover, CUDC-907 may enhance the cytotoxic effects of ABL TKI when a combined treatment strategy is used against Philadelphia chromosome-positive leukemia cells. CUDC-907 10-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 56-59 32943605-0 2020 Dual inhibition of HDAC and tyrosine kinase signaling pathways with CUDC-907 attenuates TGFbeta1 induced lung and tumor fibrosis. CUDC-907 68-76 transforming growth factor, beta 1 Mus musculus 88-96 32943605-5 2020 CUDC-907 is a first-in-class compound, functioning as a dual inhibitor of HDACs and PI3K/AKT pathway. CUDC-907 0-8 thymoma viral proto-oncogene 1 Mus musculus 89-92 32943605-8 2020 CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones. CUDC-907 0-8 thymoma viral proto-oncogene 1 Mus musculus 125-128 32943605-8 2020 CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones. CUDC-907 0-8 mechanistic target of rapamycin kinase Mus musculus 130-134 30819918-5 2019 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc. CUDC-907 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 54-59 30819918-5 2019 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc. CUDC-907 0-8 BCL2 like 11 Homo sapiens 61-64 30819918-7 2019 Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells. CUDC-907 88-96 checkpoint kinase 1 Homo sapiens 18-22 30819918-7 2019 Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells. CUDC-907 88-96 WEE1 G2 checkpoint kinase Homo sapiens 24-28 30819918-7 2019 Downregulation of CHK1, Wee1, and RRM1, and induction of DNA damage also contributed to CUDC-907-induced apoptosis of acute myeloid leukemia cells. CUDC-907 88-96 ribonucleotide reductase catalytic subunit M1 Homo sapiens 34-38 30696721-12 2019 However, a dual HDAC/PI3K inhibitor, CUDC-907, was most potent against NUT carcinoma cells, with an IC50 of 5.5-9.0 pmol/L. CUDC-907 37-45 histone deacetylase 9 Homo sapiens 16-20 30696721-20 2019 Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor). CUDC-907 63-71 delta/notch like EGF repeat containing Homo sapiens 38-41 31545402-0 2019 CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 112-115 31545402-0 2019 CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2. CUDC-907 0-8 mechanistic target of rapamycin kinase Homo sapiens 116-120 31545402-0 2019 CUDC-907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2. CUDC-907 0-8 histone deacetylase 2 Homo sapiens 135-140 31545402-4 2019 The present study aimed to explore the possibility of reversing the KF pathological phenotype using CUDC-907, a dual inhibitor of PI3K/Akt/mTOR pathway and HDACs. CUDC-907 100-108 AKT serine/threonine kinase 1 Homo sapiens 135-138 31545402-4 2019 The present study aimed to explore the possibility of reversing the KF pathological phenotype using CUDC-907, a dual inhibitor of PI3K/Akt/mTOR pathway and HDACs. CUDC-907 100-108 mechanistic target of rapamycin kinase Homo sapiens 139-143 31545402-7 2019 A mechanistic study of CUDC-907 revealed the initiation of cell cycle arrest at G2/M phase along with the enhanced expression of cyclin-dependent kinase inhibitor 1 and decreased expression of cyclin B in cells treated with CUDC-907. CUDC-907 23-31 cyclin dependent kinase inhibitor 1A Homo sapiens 129-164 31545402-7 2019 A mechanistic study of CUDC-907 revealed the initiation of cell cycle arrest at G2/M phase along with the enhanced expression of cyclin-dependent kinase inhibitor 1 and decreased expression of cyclin B in cells treated with CUDC-907. CUDC-907 224-232 cyclin dependent kinase inhibitor 1A Homo sapiens 129-164 31545402-8 2019 CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 28-31 31545402-8 2019 CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk. CUDC-907 0-8 mechanistic target of rapamycin kinase Homo sapiens 36-40 31545402-8 2019 CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk. CUDC-907 0-8 SMAD family member 2 Homo sapiens 164-171 31545402-8 2019 CUDC-907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk. CUDC-907 0-8 mitogen-activated protein kinase 1 Homo sapiens 176-179 30696721-20 2019 Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor). CUDC-907 63-71 histone deacetylase 9 Homo sapiens 46-50 30696721-20 2019 Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor). CUDC-907 63-71 histone deacetylase 9 Homo sapiens 85-89 30696721-20 2019 Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor). CUDC-907 63-71 histone deacetylase 9 Homo sapiens 85-89 30696721-20 2019 Among MYC-targeting agents, including BET and HDAC inhibitors, CUDC-907 (a dual PI3K/HDAC inhibitor) was most effective against NC cells, followed by panobinostat (an HDAC inhibitor) and AZD5153 (a bivalent BET inhibitor). CUDC-907 63-71 delta/notch like EGF repeat containing Homo sapiens 207-210 30696721-12 2019 However, a dual HDAC/PI3K inhibitor, CUDC-907, was most potent against NUT carcinoma cells, with an IC50 of 5.5-9.0 pmol/L. CUDC-907 37-45 NUT midline carcinoma family member 1 Homo sapiens 71-74 30224636-8 2019 Furthermore, we revealed the antitumor mechanism of CUDC-907 in Aspc-1, PANC-1, and Capan-1 pancreatic cancer cells: it suppressed the HDAC6 subunit, thus downregulating c-Myc protein levels, which was a mode of action distinct from the existing mechanisms. CUDC-907 52-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175 30224636-9 2019 Consistently, the extraordinary antitumor activity of CUDC-907 accompanied by downregulation of c-Myc and Ki67 expression in tumor tissue was observed in a human pancreatic cancer Aspc-1 xenograft nude mouse model in vivo. CUDC-907 54-62 MYC proto-oncogene, bHLH transcription factor Homo sapiens 96-101 30224636-0 2019 CUDC-907 displays potent antitumor activity against human pancreatic adenocarcinoma in vitro and in vivo through inhibition of HDAC6 to downregulate c-Myc expression. CUDC-907 0-8 histone deacetylase 6 Homo sapiens 127-132 30224636-0 2019 CUDC-907 displays potent antitumor activity against human pancreatic adenocarcinoma in vitro and in vivo through inhibition of HDAC6 to downregulate c-Myc expression. CUDC-907 0-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 149-154 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 24-27 30224636-4 2019 CUDC-907 is a novel dual-acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC). CUDC-907 0-8 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 45-70 30224636-8 2019 Furthermore, we revealed the antitumor mechanism of CUDC-907 in Aspc-1, PANC-1, and Capan-1 pancreatic cancer cells: it suppressed the HDAC6 subunit, thus downregulating c-Myc protein levels, which was a mode of action distinct from the existing mechanisms. CUDC-907 52-60 histone deacetylase 6 Homo sapiens 135-140 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 mitogen-activated protein kinase kinase 7 Homo sapiens 84-87 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 mitogen-activated protein kinase 1 Homo sapiens 88-91 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 signal transducer and activator of transcription 3 Homo sapiens 96-101 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 BCL2 apoptosis regulator Homo sapiens 158-163 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 BCL2 apoptosis regulator Homo sapiens 180-185 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 BCL2 like 1 Homo sapiens 187-193 30353642-4 2019 CUDC-907 inhibited PI3K/AKT and HDAC activity, as expected, but also suppressed RAF/MEK/ERK and STAT3 signalling and reduced the expression of anti-apoptotic BCL-2 family proteins BCL-2, BCL-xL, and MCL-1. CUDC-907 0-8 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 199-204 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 TNF superfamily member 13b Homo sapiens 43-47 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 TNF receptor superfamily member 13C Homo sapiens 78-83 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 TNF receptor superfamily member 13B Homo sapiens 85-89 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 TNF receptor superfamily member 17 Homo sapiens 95-99 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 TNF superfamily member 13b Homo sapiens 78-82 30353642-5 2019 Moreover, CUDC-907 downregulated cytokines BAFF and APRIL and their receptors BAFFR, TACI, and BCMA, thus blocking BAFF-induced NF-kappaB signalling. CUDC-907 10-18 nuclear factor kappa B subunit 1 Homo sapiens 128-137 30353642-6 2019 T cell chemokines CCL3/4/17/22 and phosphorylation of CXCR4 were also reduced by CUDC-907. CUDC-907 81-89 C-C motif chemokine ligand 3 Homo sapiens 18-30 30353642-6 2019 T cell chemokines CCL3/4/17/22 and phosphorylation of CXCR4 were also reduced by CUDC-907. CUDC-907 81-89 C-X-C motif chemokine receptor 4 Homo sapiens 54-59 30353642-8 2019 Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect. CUDC-907 46-54 BCL2 apoptosis regulator Homo sapiens 74-78 30353642-8 2019 Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect. CUDC-907 46-54 Bruton tyrosine kinase Homo sapiens 80-83 30353642-8 2019 Indeed, combinations of low concentrations of CUDC-907 with inhibitors of BCL2, BTK, or the NF-kappaB pathway showed a potent synergistic effect. CUDC-907 46-54 nuclear factor kappa B subunit 1 Homo sapiens 92-101 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 32-40 nuclear factor kappa B subunit 1 Homo sapiens 68-76 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 32-40 forkhead box M1 Homo sapiens 77-92 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 32-40 nuclear factor kappa B subunit 1 Homo sapiens 196-204 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 32-40 forkhead box M1 Homo sapiens 94-99 28819699-0 2018 CUDC-907, a dual HDAC and PI3K inhibitor, reverses platinum drug resistance. CUDC-907 0-8 histone deacetylase 9 Homo sapiens 17-21 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 32-40 forkhead box M1 Homo sapiens 205-210 29760046-5 2018 The radiosensitizing effects of CUDC-907 were mediated by decreased NFkappaB/Forkhead box M1 (FOXM1) recruitment to promoters of genes involved in the DNA damage response; exogenous expression of NFkappaB/FOXM1 protected from CUDC-907-induced cytotoxicity. CUDC-907 226-234 nuclear factor kappa B subunit 1 Homo sapiens 196-204 28819699-3 2018 CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 histone deacetylase 9 Homo sapiens 104-123 28819699-3 2018 CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 histone deacetylase 9 Homo sapiens 125-129 28819699-3 2018 CUDC-907 is a potent molecular targeted anticancer agent, rationally designed to simultaneously inhibit histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 135-164 28819699-13 2018 In Pt-resistant cancer cells, CUDC-907 apparently circumvented the resistance through inhibition of ABCC2 and DNA repair but induction of cell cycle arrest. CUDC-907 30-38 ATP binding cassette subfamily C member 2 Homo sapiens 100-105 28819699-14 2018 In the presence of CUDC-907, cellular accumulation of Pt drugs and formation of DNA-Pt adducts were found to be increased whereas expression levels of ABCC2 and ERCC1 was inhibited in Pt-resistant cells. CUDC-907 19-27 ATP binding cassette subfamily C member 2 Homo sapiens 151-156 28819699-14 2018 In the presence of CUDC-907, cellular accumulation of Pt drugs and formation of DNA-Pt adducts were found to be increased whereas expression levels of ABCC2 and ERCC1 was inhibited in Pt-resistant cells. CUDC-907 19-27 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 161-166 28600475-4 2017 Our aim was to determine the therapeutic efficacy of simultaneously targeting these pathways in thyroid cancer with a single agent and to evaluate biomarkers of treatment response.Experimental Design: CUDC-907 is a first-in-class compound, functioning as a dual inhibitor of HDACs and the PI3K/AKT pathway. CUDC-907 201-209 thymoma viral proto-oncogene 1 Mus musculus 294-297 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 cyclin B1 Mus musculus 231-240 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 aurora kinase A Mus musculus 242-247 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 aurora kinase B Mus musculus 249-254 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 polo like kinase 1 Mus musculus 256-260 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 276-279 28600475-5 2017 We investigated its antiproliferative effect in vitro and in vivoResults: CUDC-907 significantly inhibited cellular proliferation in thyroid cancer cell lines, induced G2-M arrest with decreased levels of the checkpoint regulators cyclin B1, AURKA, AURKB, PLK1, and increased p21 and p27. CUDC-907 74-82 cyclin-dependent kinase inhibitor 1B Mus musculus 284-287 28600475-7 2017 CUDC-907 treatment caused H3 hyperacetylation and decreased HDAC2 expression. CUDC-907 0-8 histone deacetylase 2 Mus musculus 60-65 28600475-9 2017 CUDC-907 treatment reduced both p-AKT and p-ERK1/2 levels. CUDC-907 0-8 thymoma viral proto-oncogene 1 Mus musculus 34-37 27829312-0 2017 CUDC-907 Promotes Bone Marrow Adipocytic Differentiation Through Inhibition of Histone Deacetylase and Regulation of Cell Cycle. CUDC-907 0-8 histone deacetylase 9 Homo sapiens 79-98 27829312-6 2017 Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs. CUDC-907 213-221 fatty acid binding protein 4 Homo sapiens 175-180 27829312-6 2017 Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs. CUDC-907 213-221 peroxisome proliferator activated receptor gamma Homo sapiens 182-191 27829312-6 2017 Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs. CUDC-907 213-221 Kruppel like factor 15 Homo sapiens 193-198 27829312-6 2017 Chromatin immune precipitation combined with quantitative polymerase chain reaction showed significant increase in H3K9ac epigenetic marker in the promoter regions of AdipoQ, FABP4, PPARgamma, KLF15, and CEBPA in CUDC-907-treated hBMSCs. CUDC-907 213-221 CCAAT enhancer binding protein alpha Homo sapiens 204-209 27980108-6 2017 Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. CUDC-907 40-48 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-69 28147336-5 2017 CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels. CUDC-907 0-8 AKT serine/threonine kinase 1 Homo sapiens 92-95 28147336-5 2017 CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels. CUDC-907 0-8 AKT1 substrate 1 Homo sapiens 97-103 28147336-5 2017 CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels. CUDC-907 0-8 ribosomal protein S6 Homo sapiens 105-118 28147336-5 2017 CUDC-907 treatment down-regulated the phosphorylation of PI3K downstream targets, including AKT, PRAS40, S6, and 4EBP1, increased histone 3 acetylation, and decreased Myc protein levels. CUDC-907 0-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 167-170 28147336-9 2017 Collectively, these data provide a mechanistic rationale for evaluating CUDC-907 for the treatment of patients with Myc and PI3K-dependent lymphomas. CUDC-907 72-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 116-119 27980108-6 2017 Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. CUDC-907 40-48 MYC proto-oncogene, bHLH transcription factor Homo sapiens 215-218 27980108-7 2017 Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. CUDC-907 64-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 105-108 27980108-7 2017 Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. CUDC-907 64-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 160-163 26796063-0 2016 Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase. CUDC-907 67-75 histone deacetylase 9 Homo sapiens 97-116 27980108-0 2017 Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers. CUDC-907 29-37 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-55 27980108-5 2017 Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. CUDC-907 13-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 160-163 27980108-5 2017 Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. CUDC-907 13-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 175-178 27980108-5 2017 Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. CUDC-907 13-21 NUT midline carcinoma family member 1 Homo sapiens 228-231 27980108-5 2017 Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. CUDC-907 13-21 MYC proto-oncogene, bHLH transcription factor Homo sapiens 175-178 28139498-10 2017 Furthermore, CRC cells treated with CUDC-907 exhibited a higher degree of histone H3 lysine 9 acetylation (H3K9ac) and reduced AKT phosphorylation (Ser473). CUDC-907 36-44 AKT serine/threonine kinase 1 Homo sapiens 127-130 26796063-0 2016 Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase. CUDC-907 67-75 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 121-150 26796063-1 2016 CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 histone deacetylase 9 Homo sapiens 108-127 26796063-1 2016 CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 histone deacetylase 9 Homo sapiens 129-133 26796063-1 2016 CUDC-907 is a novel, dual-acting small molecule compound designed to simultaneously inhibit the activity of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K). CUDC-907 0-8 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 139-168 26796063-2 2016 Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth. CUDC-907 15-23 histone deacetylase 9 Homo sapiens 55-59 26796063-2 2016 Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth. CUDC-907 15-23 zinc fingers and homeoboxes 2 Homo sapiens 93-96 26796063-2 2016 Treatment with CUDC-907 led to sustained inhibition of HDAC and PI3K activity, inhibition of RAF-MEK-MAPK signaling pathway, and inhibition of cancer cell growth. CUDC-907 15-23 mitogen-activated protein kinase kinase 7 Homo sapiens 97-100 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 78-86 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 30-35 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 78-86 histone deacetylase 9 Homo sapiens 190-194 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 125-133 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 30-35 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 125-133 histone deacetylase 9 Homo sapiens 190-194 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 125-133 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 30-35 26796063-6 2016 In this study, we reveal that ABCG2 reduces the intracellular accumulation of CUDC-907 and confers significant resistance to CUDC-907, which leads to reduced activity of CUDC-907 to inhibit HDAC and PI3K in human cancer cells. CUDC-907 125-133 histone deacetylase 9 Homo sapiens 190-194 26796063-7 2016 Moreover, although CUDC-907 affects the transport function of ABCG2, it was not potent enough to reverse drug resistance mediated by ABCG2 or affect the expression level of ABCG2 in human cancer cells. CUDC-907 19-27 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 62-67 26796063-8 2016 Taken together, our findings indicate that ABCG2-mediated CUDC-907 resistance can have serious clinical implications and should be further investigated. CUDC-907 58-66 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 43-48 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 54-62 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 66-71 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 54-62 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 54-62 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 66-71 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 66-71 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 26796063-9 2016 More importantly, we demonstrate that the activity of CUDC-907 in ABCG2-overexpressing cancer cells can be restored by inhibiting the function of ABCG2, which provides support for the rationale of combining CUDC-907 with modulators of ABCG2 to improve the pharmacokinetics and efficacy of CUDC-907 in future treatment trials. CUDC-907 207-215 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 146-151 35291899-9 2022 Additionally, CIITA expression levels were significantly increased with pFF alpha-synuclein administration and intensified with the co-treatment of CUDC-907 and TMP-195. CUDC-907 148-156 class II transactivator Mus musculus 14-19 26796063-0 2016 Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase. CUDC-907 67-75 ATP binding cassette subfamily A member 4 Homo sapiens 6-38 26796063-0 2016 Human ATP-Binding Cassette Transporter ABCG2 Confers Resistance to CUDC-907, a Dual Inhibitor of Histone Deacetylase and Phosphatidylinositol 3-Kinase. CUDC-907 67-75 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 39-44 34776939-9 2021 The study data show that CUDC-907 (fimepinostat), a novel dual acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC), has potent inhibitory effects on HCC cell lines and primary HCC cells in vitro, Animal studies have shown that CUDC-907 can also suppress HCC cells in vivo. CUDC-907 25-33 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 83-108 34776939-9 2021 The study data show that CUDC-907 (fimepinostat), a novel dual acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC), has potent inhibitory effects on HCC cell lines and primary HCC cells in vitro, Animal studies have shown that CUDC-907 can also suppress HCC cells in vivo. CUDC-907 259-267 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 83-108 34776939-10 2021 Furthermore, we found that CUDC-907 inhibits the PI3K/AKT/mTOR pathway and downregulates the expression of c-Myc, leading to the suppression of HCC cells. CUDC-907 27-35 thymoma viral proto-oncogene 1 Mus musculus 54-57 34776939-10 2021 Furthermore, we found that CUDC-907 inhibits the PI3K/AKT/mTOR pathway and downregulates the expression of c-Myc, leading to the suppression of HCC cells. CUDC-907 27-35 mechanistic target of rapamycin kinase Mus musculus 58-62 34099621-5 2021 Upregulation of FLT3 and activation of ERK are mechanisms of resistance to gilteritinib, while activation of JAK2/STAT5 is a mechanism of resistance to CUDC-907. CUDC-907 152-160 Janus kinase 2 Homo sapiens 109-113 34099621-5 2021 Upregulation of FLT3 and activation of ERK are mechanisms of resistance to gilteritinib, while activation of JAK2/STAT5 is a mechanism of resistance to CUDC-907. CUDC-907 152-160 signal transducer and activator of transcription 5A Homo sapiens 114-119 22693356-4 2012 RESULTS: CUDC-907 potently inhibits class I PI3Ks as well as classes I and II HDAC enzymes. CUDC-907 9-17 histone deacetylase 9 Homo sapiens 78-82 22693356-5 2012 Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases. CUDC-907 49-57 histone deacetylase 9 Homo sapiens 23-27 22693356-5 2012 Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases. CUDC-907 49-57 zinc fingers and homeoboxes 2 Homo sapiens 146-149 22693356-5 2012 Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases. CUDC-907 49-57 mitogen-activated protein kinase kinase 7 Homo sapiens 151-154 22693356-5 2012 Through its integrated HDAC inhibitory activity, CUDC-907 durably inhibits the PI3K-AKT-mTOR pathway and compensatory signaling molecules such as RAF, MEK, MAPK, and STAT-3, as well as upstream receptor tyrosine kinases. CUDC-907 49-57 signal transducer and activator of transcription 3 Homo sapiens 166-172 35291899-10 2022 Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195. CUDC-907 167-175 synuclein, alpha Mus musculus 17-32 35291899-10 2022 Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195. CUDC-907 167-175 interferon gamma Mus musculus 73-82 35291899-10 2022 Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195. CUDC-907 167-175 interferon gamma Mus musculus 83-92 35291899-10 2022 Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195. CUDC-907 167-175 interleukin 16 Mus musculus 98-112 35291899-10 2022 Furthermore, pFF alpha-synuclein caused a time-dependent increase in the IFN-gamma(IFN-gamma) and interleukin-16(IL-16) levels, and that increase was potentiated with CUDC-907 and TMP-195. CUDC-907 167-175 interleukin 16 Mus musculus 113-118 35205815-7 2022 Our results show that CUDC-907 significantly inhibits NB proliferation and colony growth, induces apoptosis, blocks cell cycle progression, inhibits MYCN, and enhances H3K9Ac levels by inhibiting the PI3K/AKT signaling pathway and HDAC function. CUDC-907 22-30 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 149-153 35205815-7 2022 Our results show that CUDC-907 significantly inhibits NB proliferation and colony growth, induces apoptosis, blocks cell cycle progression, inhibits MYCN, and enhances H3K9Ac levels by inhibiting the PI3K/AKT signaling pathway and HDAC function. CUDC-907 22-30 AKT serine/threonine kinase 1 Homo sapiens 205-208 35205815-9 2022 Overall, our findings highlight that the dual inhibition of PI3K and HDAC by CUDC-907 is an effective therapeutic strategy for NB and other MYC-dependent cancers. CUDC-907 77-85 MYC proto-oncogene, bHLH transcription factor Homo sapiens 140-143 33663586-8 2021 Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner. CUDC-907 80-88 AKT serine/threonine kinase 1 Homo sapiens 0-3 33663586-8 2021 Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner. CUDC-907 80-88 BCL2 like 1 Homo sapiens 31-37 33663586-8 2021 Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner. CUDC-907 80-88 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 39-44 33663586-8 2021 Akt activity and expression of BCL-XL, MCL-1, and NF-kappaB p65 were reduced by CUDC-907 in a dose-dependent manner. CUDC-907 80-88 RELA proto-oncogene, NF-kB subunit Homo sapiens 60-63 33077264-8 2021 Notably, and during this short period, there are four HDAC inhibitor hybrids have entered different phases of clinical trials for treatment of different types of blood and solid tumors, namely; CUDC-101, CUDC-907, Tinostamustine, and Domatinostat. CUDC-907 204-212 histone deacetylase 9 Homo sapiens 54-58 33000123-10 2021 RESULTS: From a kinase inhibitor library, we identified the dual PI3K/HDAC inhibitor CUDC-907 as a potent inhibitor of murine and human corticotroph tumor ACTH secretion (EC50 1-5nM), and cell proliferation (IC50 5nM). CUDC-907 85-93 proopiomelanocortin Homo sapiens 155-159 33000123-12 2021 We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion. CUDC-907 26-34 histone deacetylase 1 Homo sapiens 48-55 33000123-12 2021 We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion. CUDC-907 26-34 proopiomelanocortin Homo sapiens 74-78 33000123-12 2021 We also demonstrated that CUDC-907 acts through HDAC1/2 inhibition at the POMC transcriptional level combined with its PI3K-mediated inhibition of corticotroph cell viability to reduce ACTH secretion. CUDC-907 26-34 pro-opiomelanocortin-alpha Mus musculus 185-189 32165486-3 2021 In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc. CUDC-907 90-98 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 123-128 32165486-3 2021 In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc. CUDC-907 90-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 193-198 32165486-5 2021 CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis. CUDC-907 0-8 checkpoint kinase 1 Homo sapiens 23-27 32165486-5 2021 CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis. CUDC-907 0-8 WEE1 G2 checkpoint kinase Homo sapiens 29-33 32165486-5 2021 CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis. CUDC-907 0-8 ribonucleotide reductase catalytic subunit M1 Homo sapiens 35-39 32165486-5 2021 CUDC-907 downregulates CHK1, Wee1, RRM1, and c-Myc, which were found to play a role in venetoclax-induced apoptosis. CUDC-907 0-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 45-50 33757580-15 2021 The dual HDAC and PI3K inhibitor, CUDC-907, exhibited cytotoxic and immunotherapy-enhancing effects in MM cells, including multi-drug-resistant lines and primary cells from lenalidomide-resistant patients. CUDC-907 34-42 histone deacetylase 9 Homo sapiens 9-13 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 AKT serine/threonine kinase 1 Homo sapiens 74-77 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 ribosomal protein S6 Homo sapiens 83-103 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 mitogen-activated protein kinase 1 Homo sapiens 110-113 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 mitogen-activated protein kinase 1 Homo sapiens 115-153 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 180-209 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 mechanistic target of rapamycin kinase Homo sapiens 212-216 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 mechanistic target of rapamycin kinase Homo sapiens 218-247 33392641-12 2021 Furthermore, long-term treatment with CUDC-907 induced phosphorylation of AKT, S6 (ribosomal protein S6), and ERK (extracellular regulated protein kinase), and inhibition of PI3K (phosphatidylinositol 3-kinase), mTOR (mammalian target of rapamycin), or ERK significantly enhanced CUDC-907-induced cell death in pancreatic cell lines. CUDC-907 38-46 mitogen-activated protein kinase 1 Homo sapiens 253-256 33280267-4 2021 Here we performed high-throughput compound screening (HTS) using this PSC-derived NNS model to find potential therapeutic candidates and identified CUDC-907 as an effective inhibitor of the release of MCP-1 and IP-10. CUDC-907 148-156 C-C motif chemokine ligand 2 Homo sapiens 201-206 33280267-4 2021 Here we performed high-throughput compound screening (HTS) using this PSC-derived NNS model to find potential therapeutic candidates and identified CUDC-907 as an effective inhibitor of the release of MCP-1 and IP-10. CUDC-907 148-156 C-X-C motif chemokine ligand 10 Homo sapiens 211-216 33402194-0 2021 Correction to: The dual HDAC-PI3K inhibitor CUDC-907 displays single-agent activity and synergizes with PARP inhibitor olaparib in small cell lung cancer. CUDC-907 44-52 poly(ADP-ribose) polymerase 1 Homo sapiens 104-108