OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1
Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer an...
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Veröffentlicht in: | International journal of clinical and experimental pathology 2019-01, Vol.12 (7), p.2801-2808 |
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creator | Xu, Chunfeng Yan, Tingyuan Yang, Jianrong |
description | Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer and prostate cancer.
To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis.
The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells.
OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC. |
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To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis.
The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells.
OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC.</description><identifier>EISSN: 1936-2625</identifier><identifier>PMID: 31934116</identifier><language>eng</language><publisher>United States: e-Century Publishing Corporation</publisher><subject>Original</subject><ispartof>International journal of clinical and experimental pathology, 2019-01, Vol.12 (7), p.2801-2808</ispartof><rights>IJCEP Copyright © 2019.</rights><rights>IJCEP Copyright © 2019 2019</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949574/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949574/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31934116$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Chunfeng</creatorcontrib><creatorcontrib>Yan, Tingyuan</creatorcontrib><creatorcontrib>Yang, Jianrong</creatorcontrib><title>OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1</title><title>International journal of clinical and experimental pathology</title><addtitle>Int J Clin Exp Pathol</addtitle><description>Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer and prostate cancer.
To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis.
The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells.
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To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis.
The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells.
OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC.</abstract><cop>United States</cop><pub>e-Century Publishing Corporation</pub><pmid>31934116</pmid><tpages>8</tpages></addata></record> |
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title | OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1 |
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