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

• Published in: Oncology reports Vol. 37; no. 4; pp. 2087 - 2094
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.04.2017; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Apoptosis - genetics; Cancer; Care and treatment; Cell growth; Cell Line, Tumor; Cell Proliferation - genetics; Development and progression; Esophagus; Female; Gene Expression Regulation, Neoplastic; Genes; Genetic aspects; Genetic regulation; Health aspects; Humans; JAG1; Jagged-1 Protein - biosynthesis; Jagged-1 Protein - genetics; lncRNA; Lung cancer; MALAT1; Male; Medical prognosis; Medical research; Metastasis; MicroRNA; MicroRNAs; MicroRNAs - biosynthesis; MicroRNAs - genetics; miR-124; Oral cancer; Proteins; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Studies; Tongue; Tongue cancer; Tongue Neoplasms - genetics; Tongue Neoplasms - pathology; United States > US
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2017.5445

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.