Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2016
MALAT1 induces tongue cancer cells' EMT and inhibits apoptosis through Wnt/β-catenin signaling pathway.
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Liang Jun, Liang Lizhong, Ouyang Kexiong, Li Zhiqiang, Yi Xianping
Аннотация
BACKGROUND: MALAT1 is recognized as an oncogenic lncRNA 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 MALAT1 in TSCC tissues and cells.
MATERIALS AND METHODS: qPCR was performed to detect the expression of MALAT1. MALAT1 was suppressed and upregulated by plasmid transfection in TSCC cells, and then cell migration, invasion, EMT, and apoptosis were analyzed.
RESULTS: LncRNA MALAT1 was upregulated in TSCC tissues and correlated with cervical lymph node metastasis in TSCC patients. Moreover, MALAT1 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 MALAT1.
CONCLUSION: In summary, upregulated MALAT1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β-catenin signaling pathway.
MATERIALS AND METHODS: qPCR was performed to detect the expression of MALAT1. MALAT1 was suppressed and upregulated by plasmid transfection in TSCC cells, and then cell migration, invasion, EMT, and apoptosis were analyzed.
RESULTS: LncRNA MALAT1 was upregulated in TSCC tissues and correlated with cervical lymph node metastasis in TSCC patients. Moreover, MALAT1 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 MALAT1.
CONCLUSION: In summary, upregulated MALAT1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β-catenin signaling pathway.