Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells
Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hoshino, Isamu [verfasserIn] Akutsu, Yasunori [verfasserIn] Murakami, Kentaro [verfasserIn] Akanuma, Naoki [verfasserIn] Isozaki, Yuka [verfasserIn] Maruyama, Tetsuro [verfasserIn] Toyozumi, Takeshi [verfasserIn] Matsumoto, Yasunori [verfasserIn] Suito, Hiroshi [verfasserIn] Takahashi, Masahiko [verfasserIn] Sekino, Nobufumi [verfasserIn] Komatsu, Aki [verfasserIn] Suzuki, Takayoshi [verfasserIn] Matsubara, Hisahiro [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
Esophageal Squamous Cell Carcinoma |
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| Übergeordnetes Werk: |
Enthalten in: Annals of surgical oncology - Berlin [u.a.] : Springer, 1994, 23(2015), 1 vom: 20. März, Seite 312-320 |
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| Übergeordnetes Werk: |
volume:23 ; year:2015 ; number:1 ; day:20 ; month:03 ; pages:312-320 |
| Links: |
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| DOI / URN: |
10.1245/s10434-015-4488-1 |
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| Katalog-ID: |
SPR009975225 |
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| 100 | 1 | |a Hoshino, Isamu |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
| 264 | 1 | |c 2015 | |
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| 520 | |a Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. | ||
| 650 | 4 | |a Esophageal Squamous Cell Carcinoma |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Esophageal Squamous Cell Carcinoma Cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Esophageal Squamous Cell Carcinoma |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Normal Esophageal Epithelium |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a LSD1 Inhibitor |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Akutsu, Yasunori |e verfasserin |4 aut | |
| 700 | 1 | |a Murakami, Kentaro |e verfasserin |4 aut | |
| 700 | 1 | |a Akanuma, Naoki |e verfasserin |4 aut | |
| 700 | 1 | |a Isozaki, Yuka |e verfasserin |4 aut | |
| 700 | 1 | |a Maruyama, Tetsuro |e verfasserin |4 aut | |
| 700 | 1 | |a Toyozumi, Takeshi |e verfasserin |4 aut | |
| 700 | 1 | |a Matsumoto, Yasunori |e verfasserin |4 aut | |
| 700 | 1 | |a Suito, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Takahashi, Masahiko |e verfasserin |4 aut | |
| 700 | 1 | |a Sekino, Nobufumi |e verfasserin |4 aut | |
| 700 | 1 | |a Komatsu, Aki |e verfasserin |4 aut | |
| 700 | 1 | |a Suzuki, Takayoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Matsubara, Hisahiro |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Annals of surgical oncology |d Berlin [u.a.] : Springer, 1994 |g 23(2015), 1 vom: 20. März, Seite 312-320 |w (DE-627)343969947 |w (DE-600)2074021-9 |x 1534-4681 |7 nnns |
| 773 | 1 | 8 | |g volume:23 |g year:2015 |g number:1 |g day:20 |g month:03 |g pages:312-320 |
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10.1245/s10434-015-4488-1 doi (DE-627)SPR009975225 (SPR)s10434-015-4488-1-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Hoshino, Isamu verfasserin aut Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 Akutsu, Yasunori verfasserin aut Murakami, Kentaro verfasserin aut Akanuma, Naoki verfasserin aut Isozaki, Yuka verfasserin aut Maruyama, Tetsuro verfasserin aut Toyozumi, Takeshi verfasserin aut Matsumoto, Yasunori verfasserin aut Suito, Hiroshi verfasserin aut Takahashi, Masahiko verfasserin aut Sekino, Nobufumi verfasserin aut Komatsu, Aki verfasserin aut Suzuki, Takayoshi verfasserin aut Matsubara, Hisahiro verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 23(2015), 1 vom: 20. März, Seite 312-320 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:23 year:2015 number:1 day:20 month:03 pages:312-320 https://dx.doi.org/10.1245/s10434-015-4488-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 23 2015 1 20 03 312-320 |
| spelling |
10.1245/s10434-015-4488-1 doi (DE-627)SPR009975225 (SPR)s10434-015-4488-1-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Hoshino, Isamu verfasserin aut Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 Akutsu, Yasunori verfasserin aut Murakami, Kentaro verfasserin aut Akanuma, Naoki verfasserin aut Isozaki, Yuka verfasserin aut Maruyama, Tetsuro verfasserin aut Toyozumi, Takeshi verfasserin aut Matsumoto, Yasunori verfasserin aut Suito, Hiroshi verfasserin aut Takahashi, Masahiko verfasserin aut Sekino, Nobufumi verfasserin aut Komatsu, Aki verfasserin aut Suzuki, Takayoshi verfasserin aut Matsubara, Hisahiro verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 23(2015), 1 vom: 20. März, Seite 312-320 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:23 year:2015 number:1 day:20 month:03 pages:312-320 https://dx.doi.org/10.1245/s10434-015-4488-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 23 2015 1 20 03 312-320 |
| allfields_unstemmed |
10.1245/s10434-015-4488-1 doi (DE-627)SPR009975225 (SPR)s10434-015-4488-1-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Hoshino, Isamu verfasserin aut Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 Akutsu, Yasunori verfasserin aut Murakami, Kentaro verfasserin aut Akanuma, Naoki verfasserin aut Isozaki, Yuka verfasserin aut Maruyama, Tetsuro verfasserin aut Toyozumi, Takeshi verfasserin aut Matsumoto, Yasunori verfasserin aut Suito, Hiroshi verfasserin aut Takahashi, Masahiko verfasserin aut Sekino, Nobufumi verfasserin aut Komatsu, Aki verfasserin aut Suzuki, Takayoshi verfasserin aut Matsubara, Hisahiro verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 23(2015), 1 vom: 20. März, Seite 312-320 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:23 year:2015 number:1 day:20 month:03 pages:312-320 https://dx.doi.org/10.1245/s10434-015-4488-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 23 2015 1 20 03 312-320 |
| allfieldsGer |
10.1245/s10434-015-4488-1 doi (DE-627)SPR009975225 (SPR)s10434-015-4488-1-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Hoshino, Isamu verfasserin aut Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 Akutsu, Yasunori verfasserin aut Murakami, Kentaro verfasserin aut Akanuma, Naoki verfasserin aut Isozaki, Yuka verfasserin aut Maruyama, Tetsuro verfasserin aut Toyozumi, Takeshi verfasserin aut Matsumoto, Yasunori verfasserin aut Suito, Hiroshi verfasserin aut Takahashi, Masahiko verfasserin aut Sekino, Nobufumi verfasserin aut Komatsu, Aki verfasserin aut Suzuki, Takayoshi verfasserin aut Matsubara, Hisahiro verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 23(2015), 1 vom: 20. März, Seite 312-320 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:23 year:2015 number:1 day:20 month:03 pages:312-320 https://dx.doi.org/10.1245/s10434-015-4488-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 23 2015 1 20 03 312-320 |
| allfieldsSound |
10.1245/s10434-015-4488-1 doi (DE-627)SPR009975225 (SPR)s10434-015-4488-1-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Hoshino, Isamu verfasserin aut Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 Akutsu, Yasunori verfasserin aut Murakami, Kentaro verfasserin aut Akanuma, Naoki verfasserin aut Isozaki, Yuka verfasserin aut Maruyama, Tetsuro verfasserin aut Toyozumi, Takeshi verfasserin aut Matsumoto, Yasunori verfasserin aut Suito, Hiroshi verfasserin aut Takahashi, Masahiko verfasserin aut Sekino, Nobufumi verfasserin aut Komatsu, Aki verfasserin aut Suzuki, Takayoshi verfasserin aut Matsubara, Hisahiro verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 23(2015), 1 vom: 20. März, Seite 312-320 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:23 year:2015 number:1 day:20 month:03 pages:312-320 https://dx.doi.org/10.1245/s10434-015-4488-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 23 2015 1 20 03 312-320 |
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Enthalten in Annals of surgical oncology 23(2015), 1 vom: 20. März, Seite 312-320 volume:23 year:2015 number:1 day:20 month:03 pages:312-320 |
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Enthalten in Annals of surgical oncology 23(2015), 1 vom: 20. März, Seite 312-320 volume:23 year:2015 number:1 day:20 month:03 pages:312-320 |
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findex.gbv.de |
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Esophageal Squamous Cell Carcinoma Esophageal Squamous Cell Carcinoma Cell Normal Esophageal Epithelium LSD1 Inhibitor |
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Annals of surgical oncology |
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Hoshino, Isamu @@aut@@ Akutsu, Yasunori @@aut@@ Murakami, Kentaro @@aut@@ Akanuma, Naoki @@aut@@ Isozaki, Yuka @@aut@@ Maruyama, Tetsuro @@aut@@ Toyozumi, Takeshi @@aut@@ Matsumoto, Yasunori @@aut@@ Suito, Hiroshi @@aut@@ Takahashi, Masahiko @@aut@@ Sekino, Nobufumi @@aut@@ Komatsu, Aki @@aut@@ Suzuki, Takayoshi @@aut@@ Matsubara, Hisahiro @@aut@@ |
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2015-03-20T00:00:00Z |
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Hoshino, Isamu |
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Hoshino, Isamu ddc 610 bkl 44.81 bkl 44.65 misc Esophageal Squamous Cell Carcinoma misc Esophageal Squamous Cell Carcinoma Cell misc Normal Esophageal Epithelium misc LSD1 Inhibitor Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
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610 ASE 44.81 bkl 44.65 bkl Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells Esophageal Squamous Cell Carcinoma (dpeaa)DE-He213 Esophageal Squamous Cell Carcinoma Cell (dpeaa)DE-He213 Normal Esophageal Epithelium (dpeaa)DE-He213 LSD1 Inhibitor (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 bkl 44.65 misc Esophageal Squamous Cell Carcinoma misc Esophageal Squamous Cell Carcinoma Cell misc Normal Esophageal Epithelium misc LSD1 Inhibitor |
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ddc 610 bkl 44.81 bkl 44.65 misc Esophageal Squamous Cell Carcinoma misc Esophageal Squamous Cell Carcinoma Cell misc Normal Esophageal Epithelium misc LSD1 Inhibitor |
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ddc 610 bkl 44.81 bkl 44.65 misc Esophageal Squamous Cell Carcinoma misc Esophageal Squamous Cell Carcinoma Cell misc Normal Esophageal Epithelium misc LSD1 Inhibitor |
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Annals of surgical oncology |
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Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
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Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
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Hoshino, Isamu |
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Annals of surgical oncology |
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2015 |
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Hoshino, Isamu Akutsu, Yasunori Murakami, Kentaro Akanuma, Naoki Isozaki, Yuka Maruyama, Tetsuro Toyozumi, Takeshi Matsumoto, Yasunori Suito, Hiroshi Takahashi, Masahiko Sekino, Nobufumi Komatsu, Aki Suzuki, Takayoshi Matsubara, Hisahiro |
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Hoshino, Isamu |
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10.1245/s10434-015-4488-1 |
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610 |
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verfasserin |
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histone demethylase lsd1 inhibitors prevent cell growth by regulating gene expression in esophageal squamous cell carcinoma cells |
| title_auth |
Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
| abstract |
Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. |
| abstractGer |
Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. |
| abstract_unstemmed |
Background The expression of genes can be influenced by the balance of histone acetylation and/or histone demethylation, with an imbalance of these processes possibly observed in many cancers. The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. Conclusions The present observations of the comprehensive analysis of the gene expression levels provide insight into the mechanisms underlying the antitumor effects of LSD1 inhibitors in ESCC patients. |
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Histone Demethylase LSD1 Inhibitors Prevent Cell Growth by Regulating Gene Expression in Esophageal Squamous Cell Carcinoma Cells |
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Akutsu, Yasunori Murakami, Kentaro Akanuma, Naoki Isozaki, Yuka Maruyama, Tetsuro Toyozumi, Takeshi Matsumoto, Yasunori Suito, Hiroshi Takahashi, Masahiko Sekino, Nobufumi Komatsu, Aki Suzuki, Takayoshi Matsubara, Hisahiro |
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Akutsu, Yasunori Murakami, Kentaro Akanuma, Naoki Isozaki, Yuka Maruyama, Tetsuro Toyozumi, Takeshi Matsumoto, Yasunori Suito, Hiroshi Takahashi, Masahiko Sekino, Nobufumi Komatsu, Aki Suzuki, Takayoshi Matsubara, Hisahiro |
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| doi_str |
10.1245/s10434-015-4488-1 |
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2024-07-04T03:45:01.184Z |
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The histone demethylase LSD1 inhibitor activity is associated with selective transcriptional regulation and alterations in the gene expression. However, the exact mechanisms underlying the antitumor effects of LSD1 inhibitors are not fully understood. Methods The antitumor effects of NCL1, an LSD1 inhibitor, in esophageal squamous cell cancer (ESCC) cell lines were evaluated. A comprehensive analysis of the changes in the gene expression in ESCC cell lines induced by NCL1 was carried out using a microarray analysis. A loss-of-function assay using a siRNA analysis was performed to examine the oncogenic function of the gene. Results NCL1 strongly inhibited the cell growth of T.Tn and TE2 ESCC cells and induced apoptosis. According to the microarray analysis, 81 genes in the T.Tn cells and 149 genes in the TE2 cells were up- or down-regulated 2-fold or more by NCL1 exposure. Among these genes, 27 were contained in both cell lines and exhibited similar expression patterns. PHLDB2, one of the genes down-regulated by NCL1, was overexpressed in the ESCC tumor tissues. Moreover, a high expression level of PHLDB2 was found to be significantly correlated with poor prognosis. 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