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      LncRNA LUADT1 Promotes Oral Squamous Cell Carcinoma Cell Proliferation by Regulating miR-34a/GAS1 Axis

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          Abstract

          Introduction

          The oncogenic role of lncRNA LUADT1 has been investigated only in lung cancer. This study aimed to investigate the role of LUADT1 in oral squamous cell carcinoma (OSCC).

          Patients and Methods

          The expression levels of LUADT1 in paired OSCC and non-tumor tissues from OSCC patients were determined by RT-qPCR. A 5-year follow-up study was performed to analyze the prognostic value of LUADT1 for OSCC. Dual-luciferase assay and overexpression experiments were performed to assess the interactions among LUADT1, miR-34a and GASL1. Cell proliferation was analyzed by cell proliferation assay.

          Results

          In this study, we found that LUADT1 was upregulated in OSCC and predicted poor survival. LUADT1 was predicted to interact with miR-34a, which was confirmed by dual-luciferase activity assay. However, overexpression experiments showed that they did not affect the expression of each other. Interestingly, overexpression of LUADT1 resulted in upregulation of GAS1, a target of miR-34a. Cell proliferation assay revealed that overexpression of LUADT1 and GAS1 resulted in promoted cell proliferation. MiR-34a played an opposite role and reversed the effects of LUADT1 overexpression.

          Conclusion

          LUADT1 may promote OSCC proliferation by regulating miR-34a/GAS1 axis.

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          Most cited references12

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          Oral cancer: Etiology and risk factors: A review.

          Malay Kumar, Ronak Nanavati, Tapan Modi … (2016)
          Oral cancer is the sixth most common malignancy in the world. Oral cancer is of major concern in Southeast Asia primarily because of the prevalent oral habits of betel quid chewing, smoking, and alcohol consumption. Despite recent advances in cancer diagnoses and therapies, the 5.year survival rate of oral cancer patients has remained at a dismal 50% in the last few decades. This paper is an overview of the various etiological agents and risk factors implicated in the development of oral cancer.
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            A novel lncRNA, LUADT1, promotes lung adenocarcinoma proliferation via the epigenetic suppression of p27

            M Qiu, Y-Y Xu, J. Wang … (2015)
            Long noncoding RNAs (lncRNAs) are known to regulate the development and progression of various cancers. However, few lncRNAs have been well characterized in lung adenocarcinoma (LUAD). Here, we identified the expression profile of lncRNAs and protein-coding genes via microarrays analysis of paired LUAD tissues and adjacent non-tumor tissues from five female non-smokes with LUAD. A total of 498 lncRNAs and 1691 protein-coding genes were differentially expressed between LUAD tissues and paired adjacent normal tissues. A novel lncRNA, LUAD transcript 1 (LUADT1), which is highly expressed in LUAD and correlates with T stage, was characterized. Both in vitro and in vivo data showed that LUADT1 knockdown significantly inhibited proliferation of LUAD cells and induced cell cycle arrest at the G0–G1 phase. Further analysis indicated that LUADT1 may regulate cell cycle progression by epigenetically inhibiting the expression of p27. RNA immunoprecipitation and chromatin immunoprecipitation assays confirmed that LUADT1 binds to SUZ12, a core component of polycomb repressive complex 2, and mediates the trimethylation of H3K27 at the promoter region of p27. The negative correlation between LUADT1 and p27 expression was confirmed in LUAD tissue samples. These data suggested that a set of lncRNAs and protein-coding genes were differentially expressed in LUAD. LUADT1 is an oncogenic lncRNA that regulates LUAD progression, suggesting that dysregulated lncRNAs may serve as key regulatory factors in LUAD progression.
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              Sirtuin-3 (SIRT3), a Novel Potential Therapeutic Target for Oral Cancer

              Turki Alhazzazi, Pachiyappan Kamarajan, Jung Joo … (2010)
              BACKGROUND Several sirtuin family members (SIRT1-7), which are evolutionarily conserved NAD-dependent deacetylases, play an important role in carcinogenesis. However, their role in oral cancer has not yet been investigated. Therefore, the objective of this study was to investigate whether sirtuins play a role in oral cancer carcinogenesis. METHODS The expression levels of all sirtuins in several oral squamous cell carcinoma (OSCC) cell lines were compared with normal human oral keratinocytes and observed that SIRT3 was highly expressed. Therefore, tissue microarrays were used to evaluate the clinical relevance of this overexpression. SIRT3 down-regulation in OSCC cell proliferation and survival was investigated and analyzed by using cell-proliferation and cell-viability assays. Ionizing radiation and cisplatin were used to investigate whether SIRT3 down-regulation could increase the sensitivity of OSCC to both treatments. To further assess the in vivo role of SIRT3 in OSCC carcinogenesis, a floor-of-mouth oral cancer murine model was used to study the effect of SIRT3 down-regulation on OSCC tumor growth in immunodeficient mice. RESULTS The current results demonstrated for the first time that SIRT3 is overexpressed in OSCC in vitro and in vivo compared with other sirtuins. Down-regulation of SIRT3 inhibited OSCC cell growth and proliferation and increased OSCC cell sensitivity to radiation and cisplatin treatments in vitro. SIRT3 down-regulation also reduced tumor burden in vivo. CONCLUSIONS The current investigation revealed a novel role for SIRT3 in oral cancer carcinogenesis as a promoter of cell proliferation and survival, thus implicating SIRT3 as a new potential therapeutic target to treat oral cancer. Cancer 2011. © 2010 American Cancer Society.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Manag Res
                Journal ID (iso-abbrev): Cancer Manag Res
                Journal ID (publisher-id): CMAR
                Journal ID (pmc): cancmanres
                Title: Cancer Management and Research
                Publisher: Dove
                ISSN (Electronic): 1179-1322
                Publication date (Electronic): 13 May 2020
                Publication date Collection: 2020
                Volume: 12
                Pages: 3401-3407
                Affiliations
                [1 ]Department of Stomatology, Tianjin Baodi Hospital , Tianjin 301800, People’s Republic of China
                [2 ]Department of Stomatology, The Second Hospital of Lianyungang , Lianyungang City, Jiangsu Province 222000, People’s Republic of China
                [3 ]Department of Oral and Maxillofacial Surgery, Jinan Stomatological Hospital , Jinan City, Shandong Province 250001, People’s Republic of China
                Author notes
                Correspondence: Yugang Sun Department of Oral and Maxillofacial Surgery, Jinan Stomatological Hospital , No. 101 Jingliu Road, Shizhong District, Jinan City, Shandong Province250001, People’s Republic of ChinaTel +86-531-86666920 Email hk0974@163.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 238830
                DOI: 10.2147/CMAR.S238830
                PMC ID: 7231779
                SO-VID: e9addd5c-22b9-43f6-a5b1-d83eea350d95
                Copyright © © 2020 Gao et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 15 November 2019
                Date accepted : 31 March 2020
                Page count
                Figures: 5, References: 17, Pages: 7
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: oral squamous cell carcinoma,luadt1,mir-34a,gas1
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: oral squamous cell carcinoma, luadt1, mir-34a, gas1

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