Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma
Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zheji...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Fan X [verfasserIn] Jin S [verfasserIn] Li Y [verfasserIn] Khadaroo PA [verfasserIn] Dai Y [verfasserIn] He L [verfasserIn] Zhou D [verfasserIn] Lin H [verfasserIn] |
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Cancer Management and Research - Dove Medical Press, 2009, (2019), Seite 8947-8963 |
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| Übergeordnetes Werk: |
year:2019 ; pages:8947-8963 |
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| 520 | |a Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations | ||
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(DE-627)DOAJ039858944 (DE-599)DOAJ9f041540a3dd41dd8916ffdb2a75aa33 DE-627 ger DE-627 rakwb eng RC254-282 Fan X verfasserin aut Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations E-cadherin HCC Genetic alterations Epigenetic alterations Neoplasms. Tumors. Oncology. Including cancer and carcinogens Jin S verfasserin aut Li Y verfasserin aut Khadaroo PA verfasserin aut Dai Y verfasserin aut He L verfasserin aut Zhou D verfasserin aut Lin H verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2019), Seite 8947-8963 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2019 pages:8947-8963 https://doaj.org/article/9f041540a3dd41dd8916ffdb2a75aa33 kostenfrei https://www.dovepress.com/genetic-and-epigenetic-regulation-of-e-cadherin-signaling-in-human-hep-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 8947-8963 |
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(DE-627)DOAJ039858944 (DE-599)DOAJ9f041540a3dd41dd8916ffdb2a75aa33 DE-627 ger DE-627 rakwb eng RC254-282 Fan X verfasserin aut Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations E-cadherin HCC Genetic alterations Epigenetic alterations Neoplasms. Tumors. Oncology. Including cancer and carcinogens Jin S verfasserin aut Li Y verfasserin aut Khadaroo PA verfasserin aut Dai Y verfasserin aut He L verfasserin aut Zhou D verfasserin aut Lin H verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2019), Seite 8947-8963 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2019 pages:8947-8963 https://doaj.org/article/9f041540a3dd41dd8916ffdb2a75aa33 kostenfrei https://www.dovepress.com/genetic-and-epigenetic-regulation-of-e-cadherin-signaling-in-human-hep-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 8947-8963 |
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(DE-627)DOAJ039858944 (DE-599)DOAJ9f041540a3dd41dd8916ffdb2a75aa33 DE-627 ger DE-627 rakwb eng RC254-282 Fan X verfasserin aut Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations E-cadherin HCC Genetic alterations Epigenetic alterations Neoplasms. Tumors. Oncology. Including cancer and carcinogens Jin S verfasserin aut Li Y verfasserin aut Khadaroo PA verfasserin aut Dai Y verfasserin aut He L verfasserin aut Zhou D verfasserin aut Lin H verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2019), Seite 8947-8963 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2019 pages:8947-8963 https://doaj.org/article/9f041540a3dd41dd8916ffdb2a75aa33 kostenfrei https://www.dovepress.com/genetic-and-epigenetic-regulation-of-e-cadherin-signaling-in-human-hep-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 8947-8963 |
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(DE-627)DOAJ039858944 (DE-599)DOAJ9f041540a3dd41dd8916ffdb2a75aa33 DE-627 ger DE-627 rakwb eng RC254-282 Fan X verfasserin aut Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations E-cadherin HCC Genetic alterations Epigenetic alterations Neoplasms. Tumors. Oncology. Including cancer and carcinogens Jin S verfasserin aut Li Y verfasserin aut Khadaroo PA verfasserin aut Dai Y verfasserin aut He L verfasserin aut Zhou D verfasserin aut Lin H verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2019), Seite 8947-8963 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2019 pages:8947-8963 https://doaj.org/article/9f041540a3dd41dd8916ffdb2a75aa33 kostenfrei https://www.dovepress.com/genetic-and-epigenetic-regulation-of-e-cadherin-signaling-in-human-hep-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 8947-8963 |
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Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations |
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Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations |
| abstract_unstemmed |
Xiaoxiao Fan,1,* Shengxi Jin,1,2,* Yirun Li,1 Parikshit Asutosh Khadaroo,2,3 Yili Dai,1,2 Lifeng He,1 Daizhan Zhou,1 Hui Lin1 1Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 3School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia*These authors contributed equally to this workCorrespondence: Hui Lin; Daizhan ZhouDepartment of General Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 East Qingchun Road, Hangzhou 310016, People’s Republic of ChinaTel +86-13738055489; +86-21-61569704Fax +86-571-86044817; +86-21-61569704Email 369369zju.edu.cn; zhoudaizhan@gmail.comAbstract: E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-to-mesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.Keywords: E-cadherin, HCC, genetic alterations, epigenetic alterations |
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Genetic And Epigenetic Regulation Of E-Cadherin Signaling In Human Hepatocellular Carcinoma |
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