SETD2, an epigenetic tumor suppressor: a focused review on GI tumor
Significant progress has been made in our understanding of the role of epigenetic modifiers in many types of human cancer. Here, we review currently available studies on the unique histone methyltransferase, SETD2, which is responsible for H3 lysine 36 tri-methylation (H3K36me3). SETD2 plays pivotal...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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IMR Press
2020-01-01
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| Series: | Frontiers in Bioscience-Landmark |
| Subjects: | |
| Online Access: | https://www.imrpress.com/journal/FBL/25/4/10.2741/4834 |
| _version_ | 1818242651008270336 |
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| author | Ming Hu Mu Hu Qin Zhang Jin-ping Lai Xiu-li Liu |
| author_facet | Ming Hu Mu Hu Qin Zhang Jin-ping Lai Xiu-li Liu |
| author_sort | Ming Hu |
| collection | DOAJ |
| description | Significant progress has been made in our understanding of the role of epigenetic modifiers in many types of human cancer. Here, we review currently available studies on the unique histone methyltransferase, SETD2, which is responsible for H3 lysine 36 tri-methylation (H3K36me3). SETD2 plays pivotal roles in RNA alternative splicing regulation, DNA damage repair, and cytoskeleton protein methylation; inactivation of SETD2 and resultant dysregulation of these functions may lead to tumorigenesis. Despite being a newly discovered tumor suppressor, SETD2 has been found to be mutated in multiple types of cancer, including gastrointestinal tumor. Some tumors can acquire a selective growth advantage after SETD2 inactivation, which could happen in different stages in tumor progression. Decreased level of H3K36me3 caused by SETD2 inactivation has been shown to associate with higher tumor grade, tumor stage, metastasis risk, and shorter survival. Some studies also suggest that SETD2 mutation is associated with therapy resistance, therefore these SETD2-deficient tumors may need different therapeutic strategies. |
| first_indexed | 2024-12-12T13:48:37Z |
| format | Article |
| id | doaj.art-65ce75036cbf4381a864ca35ffe5e813 |
| institution | Directory Open Access Journal |
| issn | 2768-6701 |
| language | English |
| last_indexed | 2024-12-12T13:48:37Z |
| publishDate | 2020-01-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Frontiers in Bioscience-Landmark |
| spelling | doaj.art-65ce75036cbf4381a864ca35ffe5e8132022-12-22T00:22:37ZengIMR PressFrontiers in Bioscience-Landmark2768-67012020-01-0125478179710.2741/4834FBS-25-780SETD2, an epigenetic tumor suppressor: a focused review on GI tumorMing Hu0Mu Hu1Qin Zhang2Jin-ping Lai3Xiu-li Liu4Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL 32610, USADepartment of Orthopaedics, Ruijin Hospital North, School of Medicine, Shanghai Jiaotong University, Shanghai, ChinaDepartment of Pathology, Third Central Hospital of Nankai University, Tianjin, ChinaDepartment of Pathology and Laboratory Medicine, Kaiser Permanente Sacramento Medical Center, Sacramento, CA, USADepartment of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL 32610, USASignificant progress has been made in our understanding of the role of epigenetic modifiers in many types of human cancer. Here, we review currently available studies on the unique histone methyltransferase, SETD2, which is responsible for H3 lysine 36 tri-methylation (H3K36me3). SETD2 plays pivotal roles in RNA alternative splicing regulation, DNA damage repair, and cytoskeleton protein methylation; inactivation of SETD2 and resultant dysregulation of these functions may lead to tumorigenesis. Despite being a newly discovered tumor suppressor, SETD2 has been found to be mutated in multiple types of cancer, including gastrointestinal tumor. Some tumors can acquire a selective growth advantage after SETD2 inactivation, which could happen in different stages in tumor progression. Decreased level of H3K36me3 caused by SETD2 inactivation has been shown to associate with higher tumor grade, tumor stage, metastasis risk, and shorter survival. Some studies also suggest that SETD2 mutation is associated with therapy resistance, therefore these SETD2-deficient tumors may need different therapeutic strategies.https://www.imrpress.com/journal/FBL/25/4/10.2741/4834: setd2h3k36me3rna alternative splicingtubulin methylationdna damage repairprogression and prognostic biomarkerreview |
| spellingShingle | Ming Hu Mu Hu Qin Zhang Jin-ping Lai Xiu-li Liu SETD2, an epigenetic tumor suppressor: a focused review on GI tumor Frontiers in Bioscience-Landmark : setd2 h3k36me3 rna alternative splicing tubulin methylation dna damage repair progression and prognostic biomarker review |
| title | SETD2, an epigenetic tumor suppressor: a focused review on GI tumor |
| title_full | SETD2, an epigenetic tumor suppressor: a focused review on GI tumor |
| title_fullStr | SETD2, an epigenetic tumor suppressor: a focused review on GI tumor |
| title_full_unstemmed | SETD2, an epigenetic tumor suppressor: a focused review on GI tumor |
| title_short | SETD2, an epigenetic tumor suppressor: a focused review on GI tumor |
| title_sort | setd2 an epigenetic tumor suppressor a focused review on gi tumor |
| topic | : setd2 h3k36me3 rna alternative splicing tubulin methylation dna damage repair progression and prognostic biomarker review |
| url | https://www.imrpress.com/journal/FBL/25/4/10.2741/4834 |
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