lncRNA IGKJ2‐MALLP2 suppresses LSCC proliferation, migration, invasion, and angiogenesis by sponging miR‐1911‐3p/p21
Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researc...
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| Veröffentlicht in: | Cancer science Jg. 111; H. 9; S. 3245 - 3257 |
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John Wiley & Sons, Inc
01.09.2020
John Wiley and Sons Inc |
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| Abstract | Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p. Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2, which mediates p21 expression by targeting miR‐1911‐3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC.
LncRNA IGKJ2‐MALLP2 restricts the development of laryngeal squamous cell carcinoma by competitively binding miRNA‐1911‐3p to promote the expression of p21. And it also suppresses the secretion of VEGF‐A in vitro and limits the angiogenesis activities in vitro and in vivo. The number of blood vessels is decreased in the tumors over‐expressing lncRNA IGKJ2‐MALLP2. |
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| AbstractList | Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p. Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2, which mediates p21 expression by targeting miR‐1911‐3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC. Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p. Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2, which mediates p21 expression by targeting miR‐1911‐3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC. LncRNA IGKJ2‐MALLP2 restricts the development of laryngeal squamous cell carcinoma by competitively binding miRNA‐1911‐3p to promote the expression of p21. And it also suppresses the secretion of VEGF‐A in vitro and limits the angiogenesis activities in vitro and in vivo. The number of blood vessels is decreased in the tumors over‐expressing lncRNA IGKJ2‐MALLP2. Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p. Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2, which mediates p21 expression by targeting miR‐1911‐3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC. LncRNA IGKJ2‐MALLP2 restricts the development of laryngeal squamous cell carcinoma by competitively binding miRNA‐1911‐3p to promote the expression of p21. And it also suppresses the secretion of VEGF‐A in vitro and limits the angiogenesis activities in vitro and in vivo. The number of blood vessels is decreased in the tumors over‐expressing lncRNA IGKJ2‐MALLP2. Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2-MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2-MALLP2 expression was confirmed by RT-qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2-MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual-luciferase reporter assay, the ability of miR-1911-3p to bind both IGKJ2-MALLP2 and p21 mRNA was demonstrated. IGKJ2-MALLP2 could upregulate p21 expression by competitively binding miR-1911-3p. Moreover, IGKJ2-MALLP2 effectively hindered the invasion, migration, and proliferation of AMC-HN-8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF-A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2-MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2-MALLP2, which mediates p21 expression by targeting miR-1911-3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC.Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2-MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2-MALLP2 expression was confirmed by RT-qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2-MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual-luciferase reporter assay, the ability of miR-1911-3p to bind both IGKJ2-MALLP2 and p21 mRNA was demonstrated. IGKJ2-MALLP2 could upregulate p21 expression by competitively binding miR-1911-3p. Moreover, IGKJ2-MALLP2 effectively hindered the invasion, migration, and proliferation of AMC-HN-8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF-A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2-MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2-MALLP2, which mediates p21 expression by targeting miR-1911-3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC. Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p . Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2 , which mediates p21 expression by targeting miR‐1911‐3p , was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC. |
| Author | Yang, Zhenming Li, Wenjing Liu, Ming Zhang, Jiarui Cao, Jing Xu, Licheng An, Ran Sun, Yanan Zhao, Rui Tian, Linli |
| AuthorAffiliation | 1 Department of Otorhinolaryngology, Head and Neck Surgery The Second Affiliated Hospital of Harbin Medical University Harbin China 2 The Key Laboratory of Myocardial Ischemia Ministry of Education Harbin Medical University Harbin China 3 Department of Otorhinolaryngology, Head and Neck Surgery Heilongjiang Provincial Hospital Affiliated to Harbin Institute of Technology Harbin China |
| AuthorAffiliation_xml | – name: 1 Department of Otorhinolaryngology, Head and Neck Surgery The Second Affiliated Hospital of Harbin Medical University Harbin China – name: 3 Department of Otorhinolaryngology, Head and Neck Surgery Heilongjiang Provincial Hospital Affiliated to Harbin Institute of Technology Harbin China – name: 2 The Key Laboratory of Myocardial Ischemia Ministry of Education Harbin Medical University Harbin China |
| Author_xml | – sequence: 1 givenname: Jing surname: Cao fullname: Cao, Jing organization: Harbin Medical University – sequence: 2 givenname: Zhenming surname: Yang fullname: Yang, Zhenming organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 3 givenname: Ran surname: An fullname: An, Ran organization: Heilongjiang Provincial Hospital Affiliated to Harbin Institute of Technology – sequence: 4 givenname: Jiarui surname: Zhang fullname: Zhang, Jiarui organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 5 givenname: Rui surname: Zhao fullname: Zhao, Rui organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 6 givenname: Wenjing surname: Li fullname: Li, Wenjing organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 7 givenname: Licheng surname: Xu fullname: Xu, Licheng organization: Harbin Medical University – sequence: 8 givenname: Yanan surname: Sun fullname: Sun, Yanan organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 9 givenname: Ming orcidid: 0000-0002-9693-2990 surname: Liu fullname: Liu, Ming email: liumingorg@163.com organization: The Second Affiliated Hospital of Harbin Medical University – sequence: 10 givenname: Linli surname: Tian fullname: Tian, Linli email: tianlinli78@163.com organization: The Second Affiliated Hospital of Harbin Medical University |
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| Copyright | 2020 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association 2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. |
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| SubjectTerms | Angiogenesis Biotechnology Cancer therapies Cell cycle Cell growth Cell proliferation Cyclin-dependent kinase inhibitor p21 Kinases Laryngeal carcinoma lncRNA LSCC Lymph nodes Lymphatic system Metastases Metastasis mRNA Original p21 progression Proteins RNA polymerase Squamous cell carcinoma Tumor cell lines Tumor cells Tumors Vascular endothelial growth factor Xenografts |
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| Title | lncRNA IGKJ2‐MALLP2 suppresses LSCC proliferation, migration, invasion, and angiogenesis by sponging miR‐1911‐3p/p21 |
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