Methylation of ESR1 promoter induced by SNAI2–DNMT3B complex promotes epithelial–mesenchymal transition and correlates with poor prognosis in ERα‐positive breast cancers
Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expressio...
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| Published in | MedComm (2020) Vol. 4; no. 6; pp. e403 - n/a |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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China
John Wiley & Sons, Inc
01.12.2023
John Wiley and Sons Inc Wiley |
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| ISSN | 2688-2663 2688-2663 |
| DOI | 10.1002/mco2.403 |
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| Abstract | Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC.
In an ERα‐positive BC cell, SNAI2 recruited DNMT3B to form a SNAI2‐DNMT3B combination and bound on the E‐box region of the ESR1 promoter to stimulate promoter methylation. The elevated ESR1 methylation resulted in a condensed chromatin state, transcriptional repression, and gene silencing of ESR1. Besides, SNAI2‐DNMT3B‐ESR1 also significantly facilitated the process of epithelial–mesenchymal transition and promoted the invasiveness of ERα‐positive BC cells. |
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| AbstractList | Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC. Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC. In an ERα‐positive BC cell, SNAI2 recruited DNMT3B to form a SNAI2‐DNMT3B combination and bound on the E‐box region of the ESR1 promoter to stimulate promoter methylation. The elevated ESR1 methylation resulted in a condensed chromatin state, transcriptional repression, and gene silencing of ESR1. Besides, SNAI2‐DNMT3B‐ESR1 also significantly facilitated the process of epithelial–mesenchymal transition and promoted the invasiveness of ERα‐positive BC cells. Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα-negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc-finger transcriptional factor, recruited lysine-specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα-positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and methylation, and SNAI2 promoted methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα-positive BC cells. Subsequent enrichment analysis illustrated that methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression-induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse-free survival and overall survival in ERα-positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of methylation's role in promoting epithelial-mesenchymal transition in BC. Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα-negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc-finger transcriptional factor, recruited lysine-specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα-positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα-positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression-induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse-free survival and overall survival in ERα-positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial-mesenchymal transition in BC.Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα-negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc-finger transcriptional factor, recruited lysine-specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα-positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα-positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression-induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse-free survival and overall survival in ERα-positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial-mesenchymal transition in BC. Abstract Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC. Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC. In an ERα‐positive BC cell, SNAI2 recruited DNMT3B to form a SNAI2‐DNMT3B combination and bound on the E‐box region of the ESR1 promoter to stimulate promoter methylation. The elevated ESR1 methylation resulted in a condensed chromatin state, transcriptional repression, and gene silencing of ESR1. Besides, SNAI2‐DNMT3B‐ESR1 also significantly facilitated the process of epithelial–mesenchymal transition and promoted the invasiveness of ERα‐positive BC cells. Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal methylation of cytosine phosphoric acid guanine islands in the estrogen receptor 1 (ESR1) gene promoter could silence or decrease ERα expression. In ERα‐negative BC, we previously found snail family transcriptional repressor 2 (SNAI2), a zinc‐finger transcriptional factor, recruited lysine‐specific demethylase 1 to the promoter to transcriptionally suppress ERα expression by demethylating histone H3 lysine 4 dimethylation (H3K4me2). However, the role of SNAI2 in ERα‐positive BC remains elusive. In this study, we observed a positive correlation between SNAI2 and ESR1 methylation, and SNAI2 promoted ESR1 methylation by recruiting DNA methyltransferase 3 beta (DNMT3B) rather than DNA methyltransferase 1 (DNMT1) in ERα‐positive BC cells. Subsequent enrichment analysis illustrated that ESR1 methylation is strongly correlated with cell adhesion and junction. Knocking down DNMT3B could partially reverse SNAI2 overexpression‐induced cell proliferation, migration, and invasion. Moreover, high DNMT3B expression predicted poor relapse‐free survival and overall survival in ERα‐positive BC patients. In conclusion, this study demonstrated the novel mechanisms of the ESR1 methylation mediated with the SNAI2/DNMT3B complex and enhanced awareness of ESR1 methylation's role in promoting epithelial–mesenchymal transition in BC. |
| Author | Zhang, Yong‐Qu Li, Ji‐Wei Lou, Kang‐Liang Luo, Zhong Bai, Jing‐Wen Min, Wei Zhu, Jian‐Ling Wei, Xiao‐Long Gao, Yi‐Yang Deng, Qiu‐Min Zhang, Guo‐Jun Lin, Lin‐Ling Hu, Xiao‐Yi Yu Chen, Hong |
| AuthorAffiliation | 1 Fujian Key Laboratory of Precision Diagnosis and Treatment in Breast Cancer Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China 4 Xiamen Research Center of Clinical Medicine in Breast and Thyroid Cancers Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China 8 Department of Oncology Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China 6 Department of Pathology Cancer Hospital of Shantou University Medical College Shantou P. R. China 3 Xiamen Key Laboratory of Endocrine‐Related Cancer Precision Medicine Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China 5 Department of Breast‐Thyroid‐Surgery and Cancer Center Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China 2 Department of Respiratory, Critical Care and Sleep Medicine Xiang'an Hospital of Xiamen University, School of Medicine, Xi |
| AuthorAffiliation_xml | – name: 3 Xiamen Key Laboratory of Endocrine‐Related Cancer Precision Medicine Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China – name: 8 Department of Oncology Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China – name: 6 Department of Pathology Cancer Hospital of Shantou University Medical College Shantou P. R. China – name: 4 Xiamen Research Center of Clinical Medicine in Breast and Thyroid Cancers Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China – name: 5 Department of Breast‐Thyroid‐Surgery and Cancer Center Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China – name: 2 Department of Respiratory, Critical Care and Sleep Medicine Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University Xiamen P. R. China – name: 7 Cancer Research Center of Xiamen University School of Medicine Xiamen University Xiamen P. R. China – name: 1 Fujian Key Laboratory of Precision Diagnosis and Treatment in Breast Cancer Xiang'an Hospital of Xiamen University School of Medicine Xiamen University Xiamen P. R. China |
| Author_xml | – sequence: 1 givenname: Ji‐Wei surname: Li fullname: Li, Ji‐Wei organization: Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University – sequence: 2 givenname: Qiu‐Min surname: Deng fullname: Deng, Qiu‐Min organization: Xiamen University – sequence: 3 givenname: Jian‐Ling surname: Zhu fullname: Zhu, Jian‐Ling organization: Cancer Hospital of Shantou University Medical College – sequence: 4 givenname: Wei surname: Min fullname: Min, Wei organization: Xiamen University – sequence: 5 givenname: Xiao‐Yi surname: Hu fullname: Hu, Xiao‐Yi organization: Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University – sequence: 6 givenname: Hong‐ surname: Yu Chen fullname: Yu Chen, Hong‐ organization: Xiamen University – sequence: 7 givenname: Zhong surname: Luo fullname: Luo, Zhong organization: Xiamen University – sequence: 8 givenname: Lin‐Ling surname: Lin fullname: Lin, Lin‐Ling organization: Xiamen University – sequence: 9 givenname: Xiao‐Long surname: Wei fullname: Wei, Xiao‐Long organization: Cancer Hospital of Shantou University Medical College – sequence: 10 givenname: Yong‐Qu surname: Zhang fullname: Zhang, Yong‐Qu organization: Xiamen University – sequence: 11 givenname: Kang‐Liang surname: Lou fullname: Lou, Kang‐Liang organization: Xiamen University – sequence: 12 givenname: Yi‐Yang surname: Gao fullname: Gao, Yi‐Yang organization: Xiamen University – sequence: 13 givenname: Guo‐Jun orcidid: 0000-0001-5182-5887 surname: Zhang fullname: Zhang, Guo‐Jun organization: Xiamen University – sequence: 14 givenname: Jing‐Wen orcidid: 0000-0002-2107-2746 surname: Bai fullname: Bai, Jing‐Wen email: baijingwen666@126.com organization: Xiamen University |
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| CitedBy_id | crossref_primary_10_1016_j_canlet_2025_217534 crossref_primary_10_1007_s11033_024_10091_w crossref_primary_10_1016_j_bbadis_2024_167532 |
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| Keywords | epithelial–mesenchymal transition breast cancer snail family transcriptional repressor 2 ESR1 methylation DNA methyltransferase 3 beta |
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| Snippet | Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification. Abnormal... Abstract Estrogen receptor α (ERα) serves as an essential therapeutic predictor for breast cancer (BC) patients and is regulated by epigenetic modification.... |
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| SubjectTerms | Breast cancer DNA methyltransferase 3 beta epithelial–mesenchymal transition ESR1 methylation Estrogens Medical prognosis Original snail family transcriptional repressor 2 |
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| Title | Methylation of ESR1 promoter induced by SNAI2–DNMT3B complex promotes epithelial–mesenchymal transition and correlates with poor prognosis in ERα‐positive breast cancers |
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