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MALAT 1 induces tongue cancer cells' EMT and inhibits apoptosis through Wnt/β‐catenin signaling pathway
Author(s) -
Liang Jun,
Liang Lizhong,
Ouyang Kexiong,
Li Zhiqiang,
Yi Xianping
Publication year - 2017
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12466
Subject(s) - wnt signaling pathway , apoptosis , downregulation and upregulation , cancer research , signal transduction , catenin , transfection , beta catenin , cell growth , cell , chemistry , microbiology and biotechnology , biology , cell culture , gene , biochemistry , genetics
Background MALAT 1 is recognized as an oncogenic lnc RNA in various malignancies. However, its expression and function in oral tongue squamous cell carcinoma are still unknown. This study aims to investigate the expression and function of MALAT 1 in TSCC tissues and cells. Materials and Methods qPCR was performed to detect the expression of MALAT 1. MALAT 1 was suppressed and upregulated by plasmid transfection in TSCC cells, and then cell migration, invasion, EMT , and apoptosis were analyzed. Results Lnc RNA MALAT 1 was upregulated in TSCC tissues and correlated with cervical lymph node metastasis in TSCC patients. Moreover, MALAT 1 induced cell migration, invasion, EMT , and inhibited apoptosis by modulating Wnt/β‐catenin signaling pathway. Finally, inhibiting Wnt/β‐catenin signaling pathway attenuated the effect of exogenous MALAT 1. Conclusion In summary, upregulated MALAT 1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β‐catenin signaling pathway.