Silencing of LncRNA SNHG16 Downregulates Cyclin D1 (CCND1) to Abrogate Malignant Phenotypes in Oral Squamous Cell Carcinoma (OSCC) Through Upregulating miR-17-5p
| Autor: | Xieshan Huang, Pu Xu, Jingxin Han, Qiuling Wang, Deyu Liu, Xinchun Jian |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Reporter gene Oncogene Cell growth Competing endogenous RNA cyclin D1 Cell migration Biology oral squamous cell carcinoma stomatognathic diseases 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Cyclin D1 Oncology Cancer Management and Research 030220 oncology & carcinogenesis microRNA Cancer research Gene silencing competing endogenous RNA MiR-17-5p Original Research LncRNA SNHG16 |
| Zdroj: | Cancer Management and Research |
| ISSN: | 1179-1322 |
| Popis: | Qiuling Wang,1,* Jingxin Han,1,* Pu Xu,1 Xinchun Jian,1,2 Xieshan Huang,1 Deyu Liu1 1Stomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People’s Republic of China; 2Department of Oral and Maxillofacial Surgery, Xiangya Hospital, Central South University, Central South University, Changsha, Hunan, 410008, People’s Republic of China*These authors contributed equally to this workCorrespondence: Deyu LiuStomatology Center, Affiliated Haikou Hospital, Xiangya Medical College, Central South University, Renmin Road No. 43, Haikou, Hainan, 570208, People’s Republic of ChinaEmail mant3345@163.comBackground: Targeting the long non-coding RNAs (LncRNAs)-microRNAs (miRNAs)-mRNA competing endogenous RNA (ceRNA) networks has been proved as an effective strategy to treat multiple cancers, including oral squamous cell carcinoma (OSCC). Based on this, the present study identified a novel LncRNA SNHG16/miR-17-5p/CCND1 signaling pathway that played an important role in regulating the pathogenesis of OSCC.Methods: The expression levels of cancer-associated genes were examined by Real-Time qPCR and Western Blot at transcriptional and translated levels, respectively. CCK-8 assay was performed to determine cell proliferation, and cell apoptosis ratio was measured by the Annexin V-FITC/PI double staining assay. Transwell assay was performed to examine cell migration, and dual-luciferase reporter gene system assay was used to validate the ceRNA networks.Results: LncRNA SNHG16 and CCND1 were upregulated, while miR-17-5p was downregulated in OSCC tissues and cell lines, compared to their normal counterparts. Also, miR-17-5p negatively correlated with both LncRNA SNHG16 and CCND1 mRNA, but LncRNA SNHG16 was positively relevant to CCND1 mRNA in OSCC tissues. By performing the gain- and loss-of-function experiments, we noticed that LncRNA SNHG16 overexpression aggravated the malignant phenotypes, such as cell proliferation, viability, migration and epithelial-mesenchymal transition (EMT) in OSCC cells, while LncRNA SNHG16 knock-down had opposite effects. Furthermore, our dual-luciferase reporter gene system evidenced that LncRNA SNHG16 sponged miR-17-5p to upregulate CCND1 in OSCC cells, and the inhibiting effects of LncRNA SNHG16 ablation on OSCC progression were abrogated by both downregulating miR-17-5p and overexpressing CCND1. Finally, the xenograft tumor-bearing mice models were established, and our data validated that LncRNA SNHG16 served as an oncogene to promote tumorigenicity of OSCC cells in vivo.Conclusion: Taken together, targeting the LncRNA SNHG16/miR-17-5p/CCND1 axis hindered the development of OSCC, and this study provided potential diagnostic and therapeutic biomarkers for OSCC in clinic.Keywords: oral squamous cell carcinoma, competing endogenous RNA, LncRNA SNHG16, MiR-17-5p, cyclin D1 |
| Databáze: | OpenAIRE |
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