Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC
In our previous studies, enhancer of zeste homolog 2 (EZH2) has been proven to be a key oncogenic driver in oral squamous cell carcinoma (OSCC). However, the regulatory mechanisms on EZH2 remain poorly understood in OSCC. Here, through multi-transcriptomics, bioinformatics analysis, and quantitative...
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| Format: | Article |
| Language: | English |
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Elsevier
2020-06-01
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| Series: | Molecular Therapy: Nucleic Acids |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2162253120300780 |
| _version_ | 1819060237423869952 |
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| author | Kun Wu Yingying Jiang Wenkai Zhou Bolin Zhang Yan Li Fei Xie Jianjun Zhang Xu Wang Ming Yan Qin Xu Zhenhu Ren Wantao Chen Wei Cao |
| author_facet | Kun Wu Yingying Jiang Wenkai Zhou Bolin Zhang Yan Li Fei Xie Jianjun Zhang Xu Wang Ming Yan Qin Xu Zhenhu Ren Wantao Chen Wei Cao |
| author_sort | Kun Wu |
| collection | DOAJ |
| description | In our previous studies, enhancer of zeste homolog 2 (EZH2) has been proven to be a key oncogenic driver in oral squamous cell carcinoma (OSCC). However, the regulatory mechanisms on EZH2 remain poorly understood in OSCC. Here, through multi-transcriptomics, bioinformatics analysis, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), the co-expression network of long noncoding RNA RC3H2 (RC3H2), microRNA-101-3p (miR-101-3p), and EZH2 were screened and validated as a competing endogenous RNA (ceRNA) mechanism in OSCC. Silencing of RC3H2 inhibited OSCC cell proliferation, colony formation, migration, and invasion in vitro and reduced the expression of EZH2 and H3K27Me3, whereas RC3H2 overexpression significantly promoted OSCC cell growth, colony formation, migration, invasion, and xenograft tumor growth in vivo and increased the expression of EZH2 and H3K27Me3. A fluorescence in situ hybridization (FISH) assay verified that RC3H2 was predominately localized to the cytoplasm. RNA pull-down and luciferase activity assays showed that miR-101-3p was physically bound to RC3H2 as well as EZH2, and its inhibitor reversed the inhibitory effect of RC3H2 knockdown on progression of OSCC. Taken together, our findings demonstrate that RC3H2 as completive endogenous RNA sponging miR-101-3p targets EZH2 and facilitates OSCC cells’ malignant behavior. |
| first_indexed | 2024-12-21T14:23:48Z |
| format | Article |
| id | doaj.art-29abe66dbcca4f269155bd728d4d0349 |
| institution | Directory Open Access Journal |
| issn | 2162-2531 |
| language | English |
| last_indexed | 2024-12-21T14:23:48Z |
| publishDate | 2020-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Molecular Therapy: Nucleic Acids |
| spelling | doaj.art-29abe66dbcca4f269155bd728d4d03492022-12-21T19:00:41ZengElsevierMolecular Therapy: Nucleic Acids2162-25312020-06-012097110Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCCKun Wu0Yingying Jiang1Wenkai Zhou2Bolin Zhang3Yan Li4Fei Xie5Jianjun Zhang6Xu Wang7Ming Yan8Qin Xu9Zhenhu Ren10Wantao Chen11Wei Cao12Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China; Department of Dentistry, Affiliated Hospital, Weifang Medical University, Weifang 261031, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, ChinaDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Corresponding author: Zhenhu Ren, Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, No. 639, Zhizaoju Road, Shanghai, 200011, China.Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China; Corresponding author: Wantao Chen, Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, No. 639, Zhizaoju Road, Shanghai 200011, China.Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China; Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of Stomatology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China; Corresponding author: Wei Cao, Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, No. 639, Zhizaoju Road, Shanghai 200011, China.In our previous studies, enhancer of zeste homolog 2 (EZH2) has been proven to be a key oncogenic driver in oral squamous cell carcinoma (OSCC). However, the regulatory mechanisms on EZH2 remain poorly understood in OSCC. Here, through multi-transcriptomics, bioinformatics analysis, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), the co-expression network of long noncoding RNA RC3H2 (RC3H2), microRNA-101-3p (miR-101-3p), and EZH2 were screened and validated as a competing endogenous RNA (ceRNA) mechanism in OSCC. Silencing of RC3H2 inhibited OSCC cell proliferation, colony formation, migration, and invasion in vitro and reduced the expression of EZH2 and H3K27Me3, whereas RC3H2 overexpression significantly promoted OSCC cell growth, colony formation, migration, invasion, and xenograft tumor growth in vivo and increased the expression of EZH2 and H3K27Me3. A fluorescence in situ hybridization (FISH) assay verified that RC3H2 was predominately localized to the cytoplasm. RNA pull-down and luciferase activity assays showed that miR-101-3p was physically bound to RC3H2 as well as EZH2, and its inhibitor reversed the inhibitory effect of RC3H2 knockdown on progression of OSCC. Taken together, our findings demonstrate that RC3H2 as completive endogenous RNA sponging miR-101-3p targets EZH2 and facilitates OSCC cells’ malignant behavior.http://www.sciencedirect.com/science/article/pii/S2162253120300780EZH2lncRNA RC3H2microRNA-101-3pproliferationmigrationinvasion |
| spellingShingle | Kun Wu Yingying Jiang Wenkai Zhou Bolin Zhang Yan Li Fei Xie Jianjun Zhang Xu Wang Ming Yan Qin Xu Zhenhu Ren Wantao Chen Wei Cao Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC Molecular Therapy: Nucleic Acids EZH2 lncRNA RC3H2 microRNA-101-3p proliferation migration invasion |
| title | Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC |
| title_full | Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC |
| title_fullStr | Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC |
| title_full_unstemmed | Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC |
| title_short | Long Noncoding RNA RC3H2 Facilitates Cell Proliferation and Invasion by Targeting MicroRNA-101-3p/EZH2 Axis in OSCC |
| title_sort | long noncoding rna rc3h2 facilitates cell proliferation and invasion by targeting microrna 101 3p ezh2 axis in oscc |
| topic | EZH2 lncRNA RC3H2 microRNA-101-3p proliferation migration invasion |
| url | http://www.sciencedirect.com/science/article/pii/S2162253120300780 |
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