Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

Chang Shi‐Min; Hu Wei‐Wei

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Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

机译：长非编码RNA MALAT1促进口腔鳞状细胞癌发展通过microRNA‐125b / STAT3 axis

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Oral squamous cell carcinoma (OSCC), as the most common type of oral cancer, is responsible for almost 3% of all malignant tumors worldwide. Non‐coding RNAs such as lncRNAs and microRNAs have been involved in many cancers including OSCC. Recently, lncRNA metastasis‐associated lung adenocarcinoma transcript‐1 (MALAT1) has been reported to play an oncogenic role in OSCC metastasis. However, the underlying mechanism of MALAT1 in regulating OSCC progression remains unclear. The aim of this study was to investigate the specific role of MALAT1 in OSCC development. It was observed that MALAT1 was upregulated in OSCC cell lines. Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression. In addition, bioinformatics search was used to identify that miR‐125b was a direct target of MALAT1, which indicated a negative correlation between MALAT1 and miR‐125b. Besides these, STAT3 was predicted as a binding target of miR‐125b in OSCC. Overexpression of MALAT1 was able to suppress the tumor inhibitory effect of miR‐125b mimics via upregulating STAT3. Moreover, the function of MALAT1 in OSCC development was further investigated by using in vivo assays. The established nude mice models revealed that downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR‐125b/STAT3 axis, respectively. In conclusion, MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR‐125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment.

机译：口腔鳞状细胞癌(OSCC)为最常见的一种口腔癌症,负责几乎全世界所有恶性肿瘤的3%。非编码rna lncRNAs和小分子核糖核酸等参与了许多癌症包括OSCC。腺癌成绩单1 (MALAT1)据报道,发挥在OSCC致癌作用转移。MALAT1调节OSCC发展仍然存在不清楚。在OSCC MALAT1发展的特定角色。这是观察到MALAT1调节OSCC细胞线。OSCC细胞增殖而overexpressing MALAT1促进了OSCC进展。生物信息学搜索是用于识别米尔高125 b是MALAT1的直接目标表示MALAT1之间的负相关和米尔125 b。作为一个绑定米尔125 b在OSCC应承担的目标。过度的MALAT1能够抑制肿瘤抑制作用的米尔125 b模拟通过移植STAT3。在OSCC MALAT1进一步发展通过体内试验研究。建立裸鼠模型显示表达下调MALAT1大大抑制OSCC肿瘤增长和相对地upregualated MALAT1晋升OSCC发展通过miR量125 b / STAT3轴,分别。作为一个竞争内源性RNA(龙头)来调节STAT3的表达,吸收米尔在OSCC 125 b可以作为一种新的治疗目标在OSCC的诊断和治疗。

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来源
《Journal of Cellular Physiology》 |2018年第4期|3384-3396|共13页
作者
Chang Shi‐Min; Hu Wei‐Wei;
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作者单位

Department of StomatologyHuai'an Second People's Hospital and The Affiliated Huai'an Hospital of;

Department of StomatologyCapital Medical UniversityXicheng District,Beijing,China;

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正文语种英语
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关键词
MALAT1 gene;

机译：MALAT1基因;

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机译：Adu; Aged;; Aged, 80 and over;; Cadherins;; Carcinoma, Squamous Cell;; Cell Nucleus;; Cytoplasm;; Female;; Humans;; Laryngeal Neoplasms;; Male;; Middle Aged;; Neoplasm Staging;; Protein-Serine-Threonine Kinases;; Proto-Oncogene Proteins c-akt;; Retrospective Studies;; beta Catenin;; *成年人;; 老年人;; 老年人, 80以上;; 钙粘着糖蛋白类;; 癌, 鳞状细胞;; 细胞核;; 细胞质;; 喉肿瘤;; 肿瘤分期;; 蛋白质丝氨酸苏氨酸激酶;; 回顾性研究
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Long non‐coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA‐125b/STAT3 axis

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