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LINC00152通过调控miR-139-5p促进口腔鳞状细胞癌的生长和侵袭。

LINC00152 promotes the growth and invasion of oral squamous cell carcinoma by regulating miR-139-5p.

作者信息

Li Minghe, Ning Jun, Li Zhihong, Wang Jing, Zhao Cong, Wang Lei

机构信息

Department of Oral and Maxillofacial Surgery, School of Stomatology Hospital of Jilin University, Changchun, China.

Key Laboratory of Tooth Development and Bone Remodeling, School of Stomatology Jilin University, Changchun, China.

出版信息

Onco Targets Ther. 2018 Sep 27;11:6295-6304. doi: 10.2147/OTT.S168807. eCollection 2018.

DOI:10.2147/OTT.S168807
PMID:30310293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6166755/
Abstract

BACKGROUND

LINC00152 plays a crucial role in tumorigenesis and progression of multiple types of cancer. However, the biological significance of LINC00152 and its potential role in oral squamous cell carcinoma (OSCC) remain to be determined. In the present study, we investigated the role of LINC00152 and the underlying mechanism of its oncogenic activity in OSCC.

MATERIALS AND METHODS

The expression of LINC00152 in OSCC tissues and cell lines was detected using qRT-PCR. Cell proliferation, colony formation, migration, and invasion were measured using a cell counting kit, colony formation assay, wound healing, and transwell invasion assays, respectively. The target gene of LINC00152 was confirmed using a dual-luciferase reporter assay and qRT-PCR. A nude mouse model was established to analyze the function of LINC00152 in vivo.

RESULTS

LINC00152 expression was significantly upregulated in OSCC tissues and cell lines compared with that in normal counterparts. Upregulated LINC00152 served as an independent prognostic predictor in patients with OSCC. Moreover, knockdown of LINC00152 inhibited cell proliferation, colony formation, migration, and invasion, and suppressed the epithelial to mesenchymal transition in vitro, as well as impairing tumor growth in vivo. A mechanistic investigation indicated that LINC00152 could directly bind to miR-139-5p in OSCC. LINC00152 expression was inversely correlated with miR-139 expression in OSCC tissues.

CONCLUSION

Taken together, these results suggested that LINC00152 may function as oncogene in OSCC and could be a potential therapeutic target in patients with OSCC.

摘要

背景

LINC00152在多种癌症的肿瘤发生和进展中起着关键作用。然而,LINC00152的生物学意义及其在口腔鳞状细胞癌(OSCC)中的潜在作用仍有待确定。在本研究中,我们调查了LINC00152在OSCC中的作用及其致癌活性的潜在机制。

材料与方法

采用qRT-PCR检测LINC00152在OSCC组织和细胞系中的表达。分别使用细胞计数试剂盒、集落形成试验、伤口愈合试验和transwell侵袭试验测量细胞增殖、集落形成、迁移和侵袭。使用双荧光素酶报告基因试验和qRT-PCR确认LINC00152的靶基因。建立裸鼠模型以分析LINC00152在体内的功能。

结果

与正常组织相比,LINC00152在OSCC组织和细胞系中的表达显著上调。LINC00152上调是OSCC患者的独立预后预测指标。此外,敲低LINC00152可抑制细胞增殖、集落形成、迁移和侵袭,并在体外抑制上皮-间质转化,以及在体内损害肿瘤生长。机制研究表明,LINC00152可以在OSCC中直接与miR-139-5p结合。在OSCC组织中,LINC00152的表达与miR-139的表达呈负相关。

结论

综上所述,这些结果表明LINC00152可能作为OSCC中的癌基因发挥作用,并且可能是OSCC患者的潜在治疗靶点。

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