Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1

作者：Tonghan Zhang, Lizhong Liang, Xiaoling Liu, Jinan Wu, Kui Su, Jue‐yao Chen, Qiaoyi Zheng, Hongzhang Huang, Guiqing Liao · 发表于：Oncology Reports · 年份：2017 · DOI：10.3892/or.2017.5445 · 被引用次数：58 · 研究领域：Cancer-related molecular mechanisms research、RNA modifications and cancer、MicroRNA in disease regulation

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.