Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma
Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kui Chen [verfasserIn] Andre Gorgen [verfasserIn] Avrilynn Ding [verfasserIn] Lulu Du [verfasserIn] Keruo Jiang [verfasserIn] Yu Ding [verfasserIn] Gonzalo Sapisochin [verfasserIn] Anand Ghanekar [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Übergeordnetes Werk: |
In: Hepatology Communications - Wolters Kluwer Health/LWW, 2017, 5(2021), 7, Seite 1310-1328 |
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| Übergeordnetes Werk: |
volume:5 ; year:2021 ; number:7 ; pages:1310-1328 |
| Links: |
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| DOI / URN: |
10.1002/hep4.1701 |
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| Katalog-ID: |
DOAJ062961411 |
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| 520 | |a Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. | ||
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10.1002/hep4.1701 doi (DE-627)DOAJ062961411 (DE-599)DOAJ1027a28c80af4dc3b8ab3b7deed29c8f DE-627 ger DE-627 rakwb eng RC799-869 Kui Chen verfasserin aut Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. Diseases of the digestive system. Gastroenterology Andre Gorgen verfasserin aut Avrilynn Ding verfasserin aut Lulu Du verfasserin aut Keruo Jiang verfasserin aut Yu Ding verfasserin aut Gonzalo Sapisochin verfasserin aut Anand Ghanekar verfasserin aut In Hepatology Communications Wolters Kluwer Health/LWW, 2017 5(2021), 7, Seite 1310-1328 (DE-627)877444587 (DE-600)2881134-3 2471254X nnns volume:5 year:2021 number:7 pages:1310-1328 https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/article/1027a28c80af4dc3b8ab3b7deed29c8f kostenfrei https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/toc/2471-254X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2118 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2021 7 1310-1328 |
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10.1002/hep4.1701 doi (DE-627)DOAJ062961411 (DE-599)DOAJ1027a28c80af4dc3b8ab3b7deed29c8f DE-627 ger DE-627 rakwb eng RC799-869 Kui Chen verfasserin aut Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. Diseases of the digestive system. Gastroenterology Andre Gorgen verfasserin aut Avrilynn Ding verfasserin aut Lulu Du verfasserin aut Keruo Jiang verfasserin aut Yu Ding verfasserin aut Gonzalo Sapisochin verfasserin aut Anand Ghanekar verfasserin aut In Hepatology Communications Wolters Kluwer Health/LWW, 2017 5(2021), 7, Seite 1310-1328 (DE-627)877444587 (DE-600)2881134-3 2471254X nnns volume:5 year:2021 number:7 pages:1310-1328 https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/article/1027a28c80af4dc3b8ab3b7deed29c8f kostenfrei https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/toc/2471-254X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2118 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2021 7 1310-1328 |
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10.1002/hep4.1701 doi (DE-627)DOAJ062961411 (DE-599)DOAJ1027a28c80af4dc3b8ab3b7deed29c8f DE-627 ger DE-627 rakwb eng RC799-869 Kui Chen verfasserin aut Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. Diseases of the digestive system. Gastroenterology Andre Gorgen verfasserin aut Avrilynn Ding verfasserin aut Lulu Du verfasserin aut Keruo Jiang verfasserin aut Yu Ding verfasserin aut Gonzalo Sapisochin verfasserin aut Anand Ghanekar verfasserin aut In Hepatology Communications Wolters Kluwer Health/LWW, 2017 5(2021), 7, Seite 1310-1328 (DE-627)877444587 (DE-600)2881134-3 2471254X nnns volume:5 year:2021 number:7 pages:1310-1328 https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/article/1027a28c80af4dc3b8ab3b7deed29c8f kostenfrei https://doi.org/10.1002/hep4.1701 kostenfrei https://doaj.org/toc/2471-254X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2118 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2021 7 1310-1328 |
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RC799-869 Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma |
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dual‐specificity phosphatase 9 regulates cellular proliferation and predicts recurrence after surgery in hepatocellular carcinoma |
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Dual‐Specificity Phosphatase 9 Regulates Cellular Proliferation and Predicts Recurrence After Surgery in Hepatocellular Carcinoma |
| abstract |
Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. |
| abstractGer |
Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. |
| abstract_unstemmed |
Hepatocellular carcinoma (CC) is a common and deadly cancer with complex molecular pathogenesis. Little is known about dual‐specificity phosphatases (DUSPs) in HCC. We investigated DUSP9 expression in human HCC, associations between DUSP9 and patient outcomes, and effects of altered DUSP9 expression on HCC biology. We studied public data sets as well as 196 patients at our institution who had HCC resections. Quantitative real‐time reverse transcription polymerase chain reaction and western blot demonstrated that DUSP9 expression was increased <10‐fold in HCC compared to adjacent liver and healthy controls (P = 0.005). Kaplan‐Meier and multivariable regression analyses revealed that higher DUSP9 expression was associated with shorter disease‐free survival (high DUSP9, 1.6; 95% confidence interval, 0.9‐2.3 vs. low DUSP9, 3.4; 95% confidence interval, 1.8‐5.0 years; P = 0.04) and increased risk of recurrence (hazard ratio 1.55; 95% confidence interval, 1.01‐2.67; P = 0.05) after resection. DUSP9 complementary DNA (cDNA) was cloned using rapid amplification of cDNA ends, revealing two DUSP9 isoforms in human HCC cells. Studies of transcriptional regulation using promoter‐luciferase reporter constructs suggested that DUSP9 transcription is regulated by E26 transformation‐specific transcription factors. Proliferation of hepatic cells in vitro was enhanced by lentiviral‐mediated overexpression of DUSP9. In contrast, DUSP9 knockout HCC cells generated using clustered regularly interspaced short palindromic repeats (CRISPR) demonstrated decreased HCC proliferation and doxorubicin resistance in vitro and impaired xenograft growth in vivo. RNA sequencing, gene set enrichment, and network/pathway analysis revealed that DUSP9 knockout is associated with activation of protein kinase activity and apoptosis. Conclusion: DUSP9 regulates cell proliferation and predicts recurrence after surgery in HCC. DUSP9 may represent a novel prognostic candidate and therapeutic target. Additional studies are warranted to further explore the role and regulation of DUSP9 in HCC. |
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