Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer
Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expressio...
Ausführliche Beschreibung
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| Autor*in: |
Shiozaki, Atsushi [verfasserIn] Ariyoshi, Yosuke [verfasserIn] Iitaka, Daisuke [verfasserIn] Kosuga, Toshiyuki [verfasserIn] Shimizu, Hiroki [verfasserIn] Kudou, Michihiro [verfasserIn] Konishi, Tomoki [verfasserIn] Shoda, Katsutoshi [verfasserIn] Arita, Tomohiro [verfasserIn] Konishi, Hirotaka [verfasserIn] Komatsu, Shuhei [verfasserIn] Kubota, Takeshi [verfasserIn] Fujiwara, Hitoshi [verfasserIn] Okamoto, Kazuma [verfasserIn] Kishimoto, Mitsuo [verfasserIn] Konishi, Eiichi [verfasserIn] Marunaka, Yoshinori [verfasserIn] Ichikawa, Daisuke [verfasserIn] Otsuji, Eigo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Gastric Cancer - Springer-Verlag, 2002, 22(2018), 3 vom: 06. Sept., Seite 473-485 |
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| Übergeordnetes Werk: |
volume:22 ; year:2018 ; number:3 ; day:06 ; month:09 ; pages:473-485 |
| Links: |
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| DOI / URN: |
10.1007/s10120-018-0874-2 |
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SPR009349863 |
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| 520 | |a Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. | ||
| 650 | 4 | |a NIS |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Gastric cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a IFN |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a NF-kB |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Ariyoshi, Yosuke |e verfasserin |4 aut | |
| 700 | 1 | |a Iitaka, Daisuke |e verfasserin |4 aut | |
| 700 | 1 | |a Kosuga, Toshiyuki |e verfasserin |4 aut | |
| 700 | 1 | |a Shimizu, Hiroki |e verfasserin |4 aut | |
| 700 | 1 | |a Kudou, Michihiro |e verfasserin |4 aut | |
| 700 | 1 | |a Konishi, Tomoki |e verfasserin |4 aut | |
| 700 | 1 | |a Shoda, Katsutoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Arita, Tomohiro |e verfasserin |4 aut | |
| 700 | 1 | |a Konishi, Hirotaka |e verfasserin |4 aut | |
| 700 | 1 | |a Komatsu, Shuhei |e verfasserin |4 aut | |
| 700 | 1 | |a Kubota, Takeshi |e verfasserin |4 aut | |
| 700 | 1 | |a Fujiwara, Hitoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Okamoto, Kazuma |e verfasserin |4 aut | |
| 700 | 1 | |a Kishimoto, Mitsuo |e verfasserin |4 aut | |
| 700 | 1 | |a Konishi, Eiichi |e verfasserin |4 aut | |
| 700 | 1 | |a Marunaka, Yoshinori |e verfasserin |4 aut | |
| 700 | 1 | |a Ichikawa, Daisuke |e verfasserin |4 aut | |
| 700 | 1 | |a Otsuji, Eigo |e verfasserin |4 aut | |
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10.1007/s10120-018-0874-2 doi (DE-627)SPR009349863 (SPR)s10120-018-0874-2-e DE-627 ger DE-627 rakwb eng Shiozaki, Atsushi verfasserin aut Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. NIS (dpeaa)DE-He213 Gastric cancer (dpeaa)DE-He213 IFN (dpeaa)DE-He213 MAPK (dpeaa)DE-He213 NF-kB (dpeaa)DE-He213 Ariyoshi, Yosuke verfasserin aut Iitaka, Daisuke verfasserin aut Kosuga, Toshiyuki verfasserin aut Shimizu, Hiroki verfasserin aut Kudou, Michihiro verfasserin aut Konishi, Tomoki verfasserin aut Shoda, Katsutoshi verfasserin aut Arita, Tomohiro verfasserin aut Konishi, Hirotaka verfasserin aut Komatsu, Shuhei verfasserin aut Kubota, Takeshi verfasserin aut Fujiwara, Hitoshi verfasserin aut Okamoto, Kazuma verfasserin aut Kishimoto, Mitsuo verfasserin aut Konishi, Eiichi verfasserin aut Marunaka, Yoshinori verfasserin aut Ichikawa, Daisuke verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Gastric Cancer Springer-Verlag, 2002 22(2018), 3 vom: 06. Sept., Seite 473-485 (DE-627)SPR009286586 nnns volume:22 year:2018 number:3 day:06 month:09 pages:473-485 https://dx.doi.org/10.1007/s10120-018-0874-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 22 2018 3 06 09 473-485 |
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10.1007/s10120-018-0874-2 doi (DE-627)SPR009349863 (SPR)s10120-018-0874-2-e DE-627 ger DE-627 rakwb eng Shiozaki, Atsushi verfasserin aut Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. NIS (dpeaa)DE-He213 Gastric cancer (dpeaa)DE-He213 IFN (dpeaa)DE-He213 MAPK (dpeaa)DE-He213 NF-kB (dpeaa)DE-He213 Ariyoshi, Yosuke verfasserin aut Iitaka, Daisuke verfasserin aut Kosuga, Toshiyuki verfasserin aut Shimizu, Hiroki verfasserin aut Kudou, Michihiro verfasserin aut Konishi, Tomoki verfasserin aut Shoda, Katsutoshi verfasserin aut Arita, Tomohiro verfasserin aut Konishi, Hirotaka verfasserin aut Komatsu, Shuhei verfasserin aut Kubota, Takeshi verfasserin aut Fujiwara, Hitoshi verfasserin aut Okamoto, Kazuma verfasserin aut Kishimoto, Mitsuo verfasserin aut Konishi, Eiichi verfasserin aut Marunaka, Yoshinori verfasserin aut Ichikawa, Daisuke verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Gastric Cancer Springer-Verlag, 2002 22(2018), 3 vom: 06. Sept., Seite 473-485 (DE-627)SPR009286586 nnns volume:22 year:2018 number:3 day:06 month:09 pages:473-485 https://dx.doi.org/10.1007/s10120-018-0874-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 22 2018 3 06 09 473-485 |
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10.1007/s10120-018-0874-2 doi (DE-627)SPR009349863 (SPR)s10120-018-0874-2-e DE-627 ger DE-627 rakwb eng Shiozaki, Atsushi verfasserin aut Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. NIS (dpeaa)DE-He213 Gastric cancer (dpeaa)DE-He213 IFN (dpeaa)DE-He213 MAPK (dpeaa)DE-He213 NF-kB (dpeaa)DE-He213 Ariyoshi, Yosuke verfasserin aut Iitaka, Daisuke verfasserin aut Kosuga, Toshiyuki verfasserin aut Shimizu, Hiroki verfasserin aut Kudou, Michihiro verfasserin aut Konishi, Tomoki verfasserin aut Shoda, Katsutoshi verfasserin aut Arita, Tomohiro verfasserin aut Konishi, Hirotaka verfasserin aut Komatsu, Shuhei verfasserin aut Kubota, Takeshi verfasserin aut Fujiwara, Hitoshi verfasserin aut Okamoto, Kazuma verfasserin aut Kishimoto, Mitsuo verfasserin aut Konishi, Eiichi verfasserin aut Marunaka, Yoshinori verfasserin aut Ichikawa, Daisuke verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Gastric Cancer Springer-Verlag, 2002 22(2018), 3 vom: 06. Sept., Seite 473-485 (DE-627)SPR009286586 nnns volume:22 year:2018 number:3 day:06 month:09 pages:473-485 https://dx.doi.org/10.1007/s10120-018-0874-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 22 2018 3 06 09 473-485 |
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10.1007/s10120-018-0874-2 doi (DE-627)SPR009349863 (SPR)s10120-018-0874-2-e DE-627 ger DE-627 rakwb eng Shiozaki, Atsushi verfasserin aut Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. NIS (dpeaa)DE-He213 Gastric cancer (dpeaa)DE-He213 IFN (dpeaa)DE-He213 MAPK (dpeaa)DE-He213 NF-kB (dpeaa)DE-He213 Ariyoshi, Yosuke verfasserin aut Iitaka, Daisuke verfasserin aut Kosuga, Toshiyuki verfasserin aut Shimizu, Hiroki verfasserin aut Kudou, Michihiro verfasserin aut Konishi, Tomoki verfasserin aut Shoda, Katsutoshi verfasserin aut Arita, Tomohiro verfasserin aut Konishi, Hirotaka verfasserin aut Komatsu, Shuhei verfasserin aut Kubota, Takeshi verfasserin aut Fujiwara, Hitoshi verfasserin aut Okamoto, Kazuma verfasserin aut Kishimoto, Mitsuo verfasserin aut Konishi, Eiichi verfasserin aut Marunaka, Yoshinori verfasserin aut Ichikawa, Daisuke verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Gastric Cancer Springer-Verlag, 2002 22(2018), 3 vom: 06. Sept., Seite 473-485 (DE-627)SPR009286586 nnns volume:22 year:2018 number:3 day:06 month:09 pages:473-485 https://dx.doi.org/10.1007/s10120-018-0874-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 22 2018 3 06 09 473-485 |
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10.1007/s10120-018-0874-2 doi (DE-627)SPR009349863 (SPR)s10120-018-0874-2-e DE-627 ger DE-627 rakwb eng Shiozaki, Atsushi verfasserin aut Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. NIS (dpeaa)DE-He213 Gastric cancer (dpeaa)DE-He213 IFN (dpeaa)DE-He213 MAPK (dpeaa)DE-He213 NF-kB (dpeaa)DE-He213 Ariyoshi, Yosuke verfasserin aut Iitaka, Daisuke verfasserin aut Kosuga, Toshiyuki verfasserin aut Shimizu, Hiroki verfasserin aut Kudou, Michihiro verfasserin aut Konishi, Tomoki verfasserin aut Shoda, Katsutoshi verfasserin aut Arita, Tomohiro verfasserin aut Konishi, Hirotaka verfasserin aut Komatsu, Shuhei verfasserin aut Kubota, Takeshi verfasserin aut Fujiwara, Hitoshi verfasserin aut Okamoto, Kazuma verfasserin aut Kishimoto, Mitsuo verfasserin aut Konishi, Eiichi verfasserin aut Marunaka, Yoshinori verfasserin aut Ichikawa, Daisuke verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Gastric Cancer Springer-Verlag, 2002 22(2018), 3 vom: 06. Sept., Seite 473-485 (DE-627)SPR009286586 nnns volume:22 year:2018 number:3 day:06 month:09 pages:473-485 https://dx.doi.org/10.1007/s10120-018-0874-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 22 2018 3 06 09 473-485 |
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Shiozaki, Atsushi @@aut@@ Ariyoshi, Yosuke @@aut@@ Iitaka, Daisuke @@aut@@ Kosuga, Toshiyuki @@aut@@ Shimizu, Hiroki @@aut@@ Kudou, Michihiro @@aut@@ Konishi, Tomoki @@aut@@ Shoda, Katsutoshi @@aut@@ Arita, Tomohiro @@aut@@ Konishi, Hirotaka @@aut@@ Komatsu, Shuhei @@aut@@ Kubota, Takeshi @@aut@@ Fujiwara, Hitoshi @@aut@@ Okamoto, Kazuma @@aut@@ Kishimoto, Mitsuo @@aut@@ Konishi, Eiichi @@aut@@ Marunaka, Yoshinori @@aut@@ Ichikawa, Daisuke @@aut@@ Otsuji, Eigo @@aut@@ |
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The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. 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Shiozaki, Atsushi Ariyoshi, Yosuke Iitaka, Daisuke Kosuga, Toshiyuki Shimizu, Hiroki Kudou, Michihiro Konishi, Tomoki Shoda, Katsutoshi Arita, Tomohiro Konishi, Hirotaka Komatsu, Shuhei Kubota, Takeshi Fujiwara, Hitoshi Okamoto, Kazuma Kishimoto, Mitsuo Konishi, Eiichi Marunaka, Yoshinori Ichikawa, Daisuke Otsuji, Eigo |
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functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer |
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Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer |
| abstract |
Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. |
| abstractGer |
Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. |
| abstract_unstemmed |
Background Recent studies have described important roles for the sodium iodide symporter (NIS) in tumor behavior. The objectives of the present study were to investigate the role of NIS in the regulation of genes involved in tumor progression and the clinicopathological significance of its expression in gastric cancer (GC). Methods In human GC cell lines, knockdown experiments were conducted using NIS siRNA, and the effects on proliferation, survival, and cellular movement were analyzed. The gene expression profiles of cells were examined using a microarray analysis. An immunohistochemical analysis was performed on 145 primary tumor samples obtained from GC patients. Results NIS was strongly expressed in MKN45 and MKN74 cells. The depletion of NIS inhibited cell proliferation, migration, and invasion and induced apoptosis. The results of the microarray analysis revealed that various interferon (IFN) signaling-related genes, such as STAT1, STAT2, IRF1, and IFIT1, were up-regulated in NIS-depleted MKN45 cells. Furthermore, the down-regulation of NIS affected the phosphorylation of MAPKs and NF-kB. Immunohistochemical staining showed that NIS was primarily located in the cytoplasm or cell membranes of carcinoma cells, and its expression was related to the histological type or venous invasion. Prognostic analyses revealed that the strong expression of NIS was associated with shorter postoperative survival. Conclusions These results suggest that NIS regulates tumor progression by affecting IFN signaling, and that its strong expression is related to a worse prognosis in patients with GC. These results provide an insight into the role of NIS as a mediator and/or a biomarker for GC. |
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Ariyoshi, Yosuke Iitaka, Daisuke Kosuga, Toshiyuki Shimizu, Hiroki Kudou, Michihiro Konishi, Tomoki Shoda, Katsutoshi Arita, Tomohiro Konishi, Hirotaka Komatsu, Shuhei Kubota, Takeshi Fujiwara, Hitoshi Okamoto, Kazuma Kishimoto, Mitsuo Konishi, Eiichi Marunaka, Yoshinori Ichikawa, Daisuke Otsuji, Eigo |
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