Mechanism of lncRNA FEZF1-AS1 in promoting the occurrence and development of oral squamous cell carcinoma through targeting miR-196a
OBJECTIVE: Previous studies have demonstrated that long non-coding ribonucleic acid (lncRNA) FEZF1-AS1 acts as a cancer-promoting gene. However, no reports have investigated the role of FEZF1-AS1 in oral squamous cell carcinoma (OSCC) yet. Therefore, the aim of this study was to explore whether FEZF1-AS1 promoted the expression characteristics of OSCC by targeting miR-196a and to further elucidate the underlying mechanism of FEZF1-AS1 in promoting the metastasis of OSCC.
PATIENTS AND METHODS: The expression levels of FEZF1-AS1 and miR-196a in 42 pairs of OSCC tissues and para-carcinoma tissues were detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation of FEZF1-AS1 expression with clinical indexes and prognosis of OSCC patients was analyzed. Moreover, the expression levels of FEZF1-AS1 and miR-196a in OSCC cells were detected via qRT-PCR. FEZF1-AS1 knockdown and miR-196a over-expression models were established using lentivirus transfection in OSCC cell lines (CAL-27 and Tca8113). Subsequently, the influences of FEZF1-AS1 and miR-196a on the biological functions of OSCC cells were analyzed via Cell Counting Kit-8 (CCK-8) assay, colony formation assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay, respectively. Furthermore, the potential mechanism was explored using the Luciferase reporter gene and recovery assays.
RESULTS: The results of qRT-PCR proved that the expression level of FEZF1-AS1 in OSCC tissues was significantly higher than that of para-carcinoma tissues, and the difference was statistically significant. The pathological stage was significantly higher in patients with high-expression FEZF1-AS1 than those with low-expression FEZF1-AS1, while the overall survival rate was remarkably lower. The proliferation ability of cells in FEZF1-AS1 silencing group declined significantly when compared with the NC group. Similarly, qRT-PCR results verified that the expression of miR-196a in OSCC cell lines and tissues was significantly reduced as well. Meanwhile, the miR-196a expression was negatively correlated with FEZF1-AS1. Subsequent Luciferase reporter gene assay confirmed that overexpression of miR-196a could markedly reduce the activity of Luciferase containing wild-type FEZF1-AS1 vector rather than decrease the activity of Luciferase containing mutant-type vector or empty vector. These findings further indicated that FEZF1-AS1 could be targeted by miR-196a through this binding site. In addition, recovery assay demonstrates that there was a mutual regulatory effect between FEZF1-AS1 and miR-196a, jointly affecting the malignant progression of OSCC.
CONCLUSIONS: The expression of lncRNA FEZF1-AS1 was markedly up-regulated in OSCC, which was significantly correlated with pathological stage and poor prognosis of OSCC patients. Therefore, it was believed that FEZF1-AS1 might promote the malignant progression of OSCC by regulating miR-196a.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:23 |
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Enthalten in: |
European review for medical and pharmacological sciences - 23(2019), 15 vom: 05. Aug., Seite 6505-6515 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Xu, L [VerfasserIn] |
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Links: |
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Themen: |
FEZF1 protein, human |
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Anmerkungen: |
Date Completed 02.10.2020 Date Revised 02.10.2020 published: Print Citation Status MEDLINE |
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doi: |
10.26355/eurrev_201908_18534 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM299901688 |
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245 | 1 | 0 | |a Mechanism of lncRNA FEZF1-AS1 in promoting the occurrence and development of oral squamous cell carcinoma through targeting miR-196a |
264 | 1 | |c 2019 | |
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500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a OBJECTIVE: Previous studies have demonstrated that long non-coding ribonucleic acid (lncRNA) FEZF1-AS1 acts as a cancer-promoting gene. However, no reports have investigated the role of FEZF1-AS1 in oral squamous cell carcinoma (OSCC) yet. Therefore, the aim of this study was to explore whether FEZF1-AS1 promoted the expression characteristics of OSCC by targeting miR-196a and to further elucidate the underlying mechanism of FEZF1-AS1 in promoting the metastasis of OSCC | ||
520 | |a PATIENTS AND METHODS: The expression levels of FEZF1-AS1 and miR-196a in 42 pairs of OSCC tissues and para-carcinoma tissues were detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation of FEZF1-AS1 expression with clinical indexes and prognosis of OSCC patients was analyzed. Moreover, the expression levels of FEZF1-AS1 and miR-196a in OSCC cells were detected via qRT-PCR. FEZF1-AS1 knockdown and miR-196a over-expression models were established using lentivirus transfection in OSCC cell lines (CAL-27 and Tca8113). Subsequently, the influences of FEZF1-AS1 and miR-196a on the biological functions of OSCC cells were analyzed via Cell Counting Kit-8 (CCK-8) assay, colony formation assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay, respectively. Furthermore, the potential mechanism was explored using the Luciferase reporter gene and recovery assays | ||
520 | |a RESULTS: The results of qRT-PCR proved that the expression level of FEZF1-AS1 in OSCC tissues was significantly higher than that of para-carcinoma tissues, and the difference was statistically significant. The pathological stage was significantly higher in patients with high-expression FEZF1-AS1 than those with low-expression FEZF1-AS1, while the overall survival rate was remarkably lower. The proliferation ability of cells in FEZF1-AS1 silencing group declined significantly when compared with the NC group. Similarly, qRT-PCR results verified that the expression of miR-196a in OSCC cell lines and tissues was significantly reduced as well. Meanwhile, the miR-196a expression was negatively correlated with FEZF1-AS1. Subsequent Luciferase reporter gene assay confirmed that overexpression of miR-196a could markedly reduce the activity of Luciferase containing wild-type FEZF1-AS1 vector rather than decrease the activity of Luciferase containing mutant-type vector or empty vector. These findings further indicated that FEZF1-AS1 could be targeted by miR-196a through this binding site. In addition, recovery assay demonstrates that there was a mutual regulatory effect between FEZF1-AS1 and miR-196a, jointly affecting the malignant progression of OSCC | ||
520 | |a CONCLUSIONS: The expression of lncRNA FEZF1-AS1 was markedly up-regulated in OSCC, which was significantly correlated with pathological stage and poor prognosis of OSCC patients. Therefore, it was believed that FEZF1-AS1 might promote the malignant progression of OSCC by regulating miR-196a | ||
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700 | 1 | |a Yang, P |e verfasserin |4 aut | |
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