期刊
ONCOLOGY REPORTS
卷 37, 期 4, 页码 2087-2094出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2017.5445
关键词
lncRNA; MALAT1; miR-124; tongue cancer; JAG1
类别
资金
- National Natural Science Foundation of China [81302356]
- Postdoctoral Science Foundation of China [2012M511877]
- Scientific Projects of Zhongshan City [20122A006]
- Natural Science Foundation of Guangdong Province [2014A030310076]
- Science and Technology Project of Guangdong Province [2016A020215031]
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (IncRNA), 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, IncRNA-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 jaggedl (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.
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