Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been r...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ishikawa, Akira [verfasserIn] Fujii, Hiroki [verfasserIn] Fukui, Takafumi [verfasserIn] Kido, Aya [verfasserIn] Katsuya, Narutaka [verfasserIn] Sentani, Kazuhiro [verfasserIn] Kuraoka, Kazuya [verfasserIn] Tazuma, Sho [verfasserIn] Sudo, Takeshi [verfasserIn] Serikawa, Masahiro [verfasserIn] Oka, Shiro [verfasserIn] Oue, Naohide [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Pathology, research and practice - München : Elsevier, 1978, 241 |
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| Übergeordnetes Werk: |
volume:241 |
| DOI / URN: |
10.1016/j.prp.2022.154277 |
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| Katalog-ID: |
ELV06521675X |
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| 245 | 1 | 0 | |a Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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| 520 | |a Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. | ||
| 650 | 4 | |a Biomarker | |
| 650 | 4 | |a Cancer stem | |
| 650 | 4 | |a Kinesin family member C1 | |
| 650 | 4 | |a Pancreatic ductal cancer | |
| 700 | 1 | |a Fujii, Hiroki |e verfasserin |4 aut | |
| 700 | 1 | |a Fukui, Takafumi |e verfasserin |4 aut | |
| 700 | 1 | |a Kido, Aya |e verfasserin |4 aut | |
| 700 | 1 | |a Katsuya, Narutaka |e verfasserin |4 aut | |
| 700 | 1 | |a Sentani, Kazuhiro |e verfasserin |4 aut | |
| 700 | 1 | |a Kuraoka, Kazuya |e verfasserin |4 aut | |
| 700 | 1 | |a Tazuma, Sho |e verfasserin |4 aut | |
| 700 | 1 | |a Sudo, Takeshi |e verfasserin |4 aut | |
| 700 | 1 | |a Serikawa, Masahiro |e verfasserin |4 aut | |
| 700 | 1 | |a Oka, Shiro |e verfasserin |4 aut | |
| 700 | 1 | |a Oue, Naohide |e verfasserin |4 aut | |
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2022 |
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2022 |
| allfields |
10.1016/j.prp.2022.154277 doi (DE-627)ELV06521675X (ELSEVIER)S0344-0338(22)00521-0 DE-627 ger DE-627 rda eng 610 VZ 44.47 bkl Ishikawa, Akira verfasserin aut Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness 2022 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer Fujii, Hiroki verfasserin aut Fukui, Takafumi verfasserin aut Kido, Aya verfasserin aut Katsuya, Narutaka verfasserin aut Sentani, Kazuhiro verfasserin aut Kuraoka, Kazuya verfasserin aut Tazuma, Sho verfasserin aut Sudo, Takeshi verfasserin aut Serikawa, Masahiro verfasserin aut Oka, Shiro verfasserin aut Oue, Naohide verfasserin aut Enthalten in Pathology, research and practice München : Elsevier, 1978 241 Online-Ressource (DE-627)325789517 (DE-600)2039756-2 (DE-576)094480672 1618-0631 nnns volume:241 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.47 Pathologie Medizin VZ AR 241 |
| spelling |
10.1016/j.prp.2022.154277 doi (DE-627)ELV06521675X (ELSEVIER)S0344-0338(22)00521-0 DE-627 ger DE-627 rda eng 610 VZ 44.47 bkl Ishikawa, Akira verfasserin aut Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness 2022 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer Fujii, Hiroki verfasserin aut Fukui, Takafumi verfasserin aut Kido, Aya verfasserin aut Katsuya, Narutaka verfasserin aut Sentani, Kazuhiro verfasserin aut Kuraoka, Kazuya verfasserin aut Tazuma, Sho verfasserin aut Sudo, Takeshi verfasserin aut Serikawa, Masahiro verfasserin aut Oka, Shiro verfasserin aut Oue, Naohide verfasserin aut Enthalten in Pathology, research and practice München : Elsevier, 1978 241 Online-Ressource (DE-627)325789517 (DE-600)2039756-2 (DE-576)094480672 1618-0631 nnns volume:241 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.47 Pathologie Medizin VZ AR 241 |
| allfields_unstemmed |
10.1016/j.prp.2022.154277 doi (DE-627)ELV06521675X (ELSEVIER)S0344-0338(22)00521-0 DE-627 ger DE-627 rda eng 610 VZ 44.47 bkl Ishikawa, Akira verfasserin aut Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness 2022 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer Fujii, Hiroki verfasserin aut Fukui, Takafumi verfasserin aut Kido, Aya verfasserin aut Katsuya, Narutaka verfasserin aut Sentani, Kazuhiro verfasserin aut Kuraoka, Kazuya verfasserin aut Tazuma, Sho verfasserin aut Sudo, Takeshi verfasserin aut Serikawa, Masahiro verfasserin aut Oka, Shiro verfasserin aut Oue, Naohide verfasserin aut Enthalten in Pathology, research and practice München : Elsevier, 1978 241 Online-Ressource (DE-627)325789517 (DE-600)2039756-2 (DE-576)094480672 1618-0631 nnns volume:241 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.47 Pathologie Medizin VZ AR 241 |
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10.1016/j.prp.2022.154277 doi (DE-627)ELV06521675X (ELSEVIER)S0344-0338(22)00521-0 DE-627 ger DE-627 rda eng 610 VZ 44.47 bkl Ishikawa, Akira verfasserin aut Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness 2022 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer Fujii, Hiroki verfasserin aut Fukui, Takafumi verfasserin aut Kido, Aya verfasserin aut Katsuya, Narutaka verfasserin aut Sentani, Kazuhiro verfasserin aut Kuraoka, Kazuya verfasserin aut Tazuma, Sho verfasserin aut Sudo, Takeshi verfasserin aut Serikawa, Masahiro verfasserin aut Oka, Shiro verfasserin aut Oue, Naohide verfasserin aut Enthalten in Pathology, research and practice München : Elsevier, 1978 241 Online-Ressource (DE-627)325789517 (DE-600)2039756-2 (DE-576)094480672 1618-0631 nnns volume:241 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.47 Pathologie Medizin VZ AR 241 |
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10.1016/j.prp.2022.154277 doi (DE-627)ELV06521675X (ELSEVIER)S0344-0338(22)00521-0 DE-627 ger DE-627 rda eng 610 VZ 44.47 bkl Ishikawa, Akira verfasserin aut Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness 2022 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer Fujii, Hiroki verfasserin aut Fukui, Takafumi verfasserin aut Kido, Aya verfasserin aut Katsuya, Narutaka verfasserin aut Sentani, Kazuhiro verfasserin aut Kuraoka, Kazuya verfasserin aut Tazuma, Sho verfasserin aut Sudo, Takeshi verfasserin aut Serikawa, Masahiro verfasserin aut Oka, Shiro verfasserin aut Oue, Naohide verfasserin aut Enthalten in Pathology, research and practice München : Elsevier, 1978 241 Online-Ressource (DE-627)325789517 (DE-600)2039756-2 (DE-576)094480672 1618-0631 nnns volume:241 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.47 Pathologie Medizin VZ AR 241 |
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English |
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Enthalten in Pathology, research and practice 241 volume:241 |
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Enthalten in Pathology, research and practice 241 volume:241 |
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Pathology, research and practice |
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Ishikawa, Akira @@aut@@ Fujii, Hiroki @@aut@@ Fukui, Takafumi @@aut@@ Kido, Aya @@aut@@ Katsuya, Narutaka @@aut@@ Sentani, Kazuhiro @@aut@@ Kuraoka, Kazuya @@aut@@ Tazuma, Sho @@aut@@ Sudo, Takeshi @@aut@@ Serikawa, Masahiro @@aut@@ Oka, Shiro @@aut@@ Oue, Naohide @@aut@@ |
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2022-01-01T00:00:00Z |
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3610 |
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englisch |
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Ishikawa, Akira |
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Ishikawa, Akira ddc 610 bkl 44.47 misc Biomarker misc Cancer stem misc Kinesin family member C1 misc Pancreatic ductal cancer Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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610 VZ 44.47 bkl Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness Biomarker Cancer stem Kinesin family member C1 Pancreatic ductal cancer |
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Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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Ishikawa, Akira Fujii, Hiroki Fukui, Takafumi Kido, Aya Katsuya, Narutaka Sentani, Kazuhiro Kuraoka, Kazuya Tazuma, Sho Sudo, Takeshi Serikawa, Masahiro Oka, Shiro Oue, Naohide |
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expression of kinesin family member c1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
| abstract |
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. |
| abstractGer |
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. |
| abstract_unstemmed |
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC. |
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Expression of kinesin family member C1 in pancreatic ductal adenocarcinoma affects tumor progression and stemness |
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Fujii, Hiroki Fukui, Takafumi Kido, Aya Katsuya, Narutaka Sentani, Kazuhiro Kuraoka, Kazuya Tazuma, Sho Sudo, Takeshi Serikawa, Masahiro Oka, Shiro Oue, Naohide |
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| score |
7.4030848 |