SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter
SET domain bifurcated 1 (SETDB1) is a histone H3 lysine 9 methyltransferase that is highly expressed in various tumor types, including breast cancer. However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explor...
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| Veröffentlicht in: | Oncology reports 2019-02, Vol.41 (2), p.1284-1292 |
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| container_title | Oncology reports |
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| creator | Yang, Wenlin Su, Ying Hou, Chenjian Chen, Linlin Zhou, Danmei Ren, Kehan Zhou, Zhaoping Zhang, Renya Liu, Xiuping |
| description | SET domain bifurcated 1 (SETDB1) is a histone H3 lysine 9 methyltransferase that is highly expressed in various tumor types, including breast cancer. However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explore the role of SETDB1 in breast cancer cells. SETDB1 downregulation in BT549 and MDA‑MB‑231 cells reduced cell proliferation, whereas upregulation in MCF7 and T47D cells enhanced proliferation. Depletion of SETDB1 suppressed cell migration and invasion in vitro and reduced lung metastasis in vivo. By contrast, SETDB1 overexpression enhanced cell migration and invasiveness. Notably, SETDB1 overexpression appeared to induce epithelial‑mesenchymal transition (EMT) in MCF7 cells. Mechanistic investigations indicated that SETDB1 acts as an EMT inducer by binding directly to the promoter of the transcription factor Snail. Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer. |
| doi_str_mv | 10.3892/or.2018.6871 |
| format | Article |
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However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explore the role of SETDB1 in breast cancer cells. SETDB1 downregulation in BT549 and MDA‑MB‑231 cells reduced cell proliferation, whereas upregulation in MCF7 and T47D cells enhanced proliferation. Depletion of SETDB1 suppressed cell migration and invasion in vitro and reduced lung metastasis in vivo. By contrast, SETDB1 overexpression enhanced cell migration and invasiveness. Notably, SETDB1 overexpression appeared to induce epithelial‑mesenchymal transition (EMT) in MCF7 cells. Mechanistic investigations indicated that SETDB1 acts as an EMT inducer by binding directly to the promoter of the transcription factor Snail. Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2018.6871</identifier><identifier>PMID: 30483750</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Binding sites ; Biotechnology ; Breast cancer ; Care and treatment ; Cell growth ; CRISPR ; Development and progression ; Epigenetics ; Gene expression ; Genetic aspects ; Health aspects ; Infections ; Lung cancer ; Medical prognosis ; Metastasis ; Proteins ; Stem cells ; Transcription factors</subject><ispartof>Oncology reports, 2019-02, Vol.41 (2), p.1284-1292</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-c517ab45f446078e8e67008c1f60fa8f99c3e6c1314749614c25cc89eafb7a343</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30483750$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Wenlin</creatorcontrib><creatorcontrib>Su, Ying</creatorcontrib><creatorcontrib>Hou, Chenjian</creatorcontrib><creatorcontrib>Chen, Linlin</creatorcontrib><creatorcontrib>Zhou, Danmei</creatorcontrib><creatorcontrib>Ren, Kehan</creatorcontrib><creatorcontrib>Zhou, Zhaoping</creatorcontrib><creatorcontrib>Zhang, Renya</creatorcontrib><creatorcontrib>Liu, Xiuping</creatorcontrib><title>SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>SET domain bifurcated 1 (SETDB1) is a histone H3 lysine 9 methyltransferase that is highly expressed in various tumor types, including breast cancer. 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Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer.</description><subject>Binding sites</subject><subject>Biotechnology</subject><subject>Breast cancer</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>CRISPR</subject><subject>Development and progression</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Infections</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Proteins</subject><subject>Stem cells</subject><subject>Transcription factors</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkk1rFTEUhgdRbK3uXEtAEBfONd_JLGutVSi4aAV3IZN7pjclk1yTGcrd9S_4F_0lZtr6UZGzyCE85z0nJ2_TPCd4xXRH36a8opjoldSKPGj2iepISzkjD2uOKWkZE1_3mielXGJMFZbd42aPYa6ZEni_iWfH5-_fEeTjenZQEGz9tIHgbfhx_X2EAtFtdqMNaMo2Fj_5FCuL-gy2TMjZ7HxMo0X9Dq19BjeFHeqrmI8X6KpKobNofUDbnMY0QX7aPBpsKPDs7jxovnw4Pj_62J5-Pvl0dHjaOi7E1DpBlO25GDiXWGnQIBXG2pFB4sHqoescA-kII1zxThLuqHBOd2CHXlnG2UHz-la3Nv42Q5nM6IuDEGyENBdDCdOSdfQGffkPepnmHOt0lZK041hT8Ye6sAGMj0OqC3GLqDkUClOMmWSVWv2HqrGG0bsUYfD1_l7Bq78KNmDDtCkpzMuey33wzS3ociolw2C22Y827wzBZvGBSdksPjCLDyr-4u5Rcz_C-jf86-PZT40orGI</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Yang, Wenlin</creator><creator>Su, Ying</creator><creator>Hou, Chenjian</creator><creator>Chen, Linlin</creator><creator>Zhou, Danmei</creator><creator>Ren, Kehan</creator><creator>Zhou, Zhaoping</creator><creator>Zhang, Renya</creator><creator>Liu, Xiuping</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190201</creationdate><title>SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter</title><author>Yang, Wenlin ; 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However, how SETDB1 functions in breast cancer is unclear. In the present study, proliferation, migration and invasion assays were performed to explore the role of SETDB1 in breast cancer cells. SETDB1 downregulation in BT549 and MDA‑MB‑231 cells reduced cell proliferation, whereas upregulation in MCF7 and T47D cells enhanced proliferation. Depletion of SETDB1 suppressed cell migration and invasion in vitro and reduced lung metastasis in vivo. By contrast, SETDB1 overexpression enhanced cell migration and invasiveness. Notably, SETDB1 overexpression appeared to induce epithelial‑mesenchymal transition (EMT) in MCF7 cells. Mechanistic investigations indicated that SETDB1 acts as an EMT inducer by binding directly to the promoter of the transcription factor Snail. Thus, SETDB1 is involved in breast cancer metastasis and may be a therapeutic target for treating patients with breast cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30483750</pmid><doi>10.3892/or.2018.6871</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Binding sites Biotechnology Breast cancer Care and treatment Cell growth CRISPR Development and progression Epigenetics Gene expression Genetic aspects Health aspects Infections Lung cancer Medical prognosis Metastasis Proteins Stem cells Transcription factors |
| title | SETDB1 induces epithelial‑mesenchymal transition in breast carcinoma by directly binding with Snail promoter |
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