Zhang Tong-Han, Liang Li-Zhong, Liu Xiao-Ling, Wu Ji-Nan, Su Kui, Chen Jue-Yao, Zheng Qiao-Yi, Huang Hong-Zhang, Liao Gui-Qing
Department of Oral and Maxillofacial Surgery, The Affiliated Zhongshan Hospital, Sun Yat-sen University, Zhongshan, Guangdong 528403, P.R. China.
Department of Oral and Maxillofacial Surgery, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong 519000, P.R. China.
Oncol Rep. 2017 Apr;37(4):2087-2094. doi: 10.3892/or.2017.5445. Epub 2017 Feb 14.
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), was the earliest discovered to be correlated with cancer and contributes to the initiation and development of several types of tumors. Dysregulation of MALAT1 expression is frequently observed in many types of cancer such as gastric cancer, esophageal squamous cell carcinoma and glioma. To date, the role of MALAT1 and the underlying mechanisms in tongue cancer development remain unclear. In the present study, we studied the influence of MALAT1 on tongue cancer cell lines and clinical tongue cancer samples so as to detect its function and the underlying mechanism. In the present study, lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.
转移相关的肺腺癌转录本1（MALAT1）是一种长链非编码RNA（lncRNA），最早被发现与癌症相关，并促进多种类型肿瘤的发生和发展。在许多类型的癌症中，如胃癌、食管鳞状细胞癌和神经胶质瘤，经常观察到MALAT1表达失调。迄今为止，MALAT1在舌癌发生发展中的作用及潜在机制仍不清楚。在本研究中，我们研究了MALAT1对舌癌细胞系和临床舌癌样本的影响，以检测其功能及潜在机制。在本研究中，lncRNA-MALAT1在舌癌细胞系中特异性上调，过表达通过靶向miR-124促进舌癌细胞生长。敲低MALAT1可抑制人舌癌细胞的生长和侵袭，并在体外和体内抑制转移。此外，MALAT1诱导的舌癌细胞生长需要miR-124依赖的锯齿状蛋白1（JAG1）调节。我们的数据表明，MALAT1通过miR-124依赖的JAG1调节抑制舌癌细胞生长和转移。总之，我们揭示了MALAT1可能通过增加舌癌的增殖和转移发挥致癌作用，是人类舌癌潜在的治疗靶点。
