Decreased long non-coding RNA MTM contributes to gastric cancer cell migration and invasion via modulating MT1F
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Zhenghua Lin1,2,*, Sanchuan Lai1,2,*, Xingkang He1,2, Wei Zhuo2,3, Lan Wang1,2, Jianmin Si1,2 and Shujie Chen1,2
1Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310020, Zhejiang Province, China
2Institute of Gastroenterology, Zhejiang University, Hangzhou 310016, Zhejiang Province, China
3Department of Cell Biology and Program in Molecular Cell Biology, Zhejiang University School of Medicine, Hangzhou 310058, Zhejiang Province, China
*These authors have contributed equally to this work
Shujie Chen, email: email@example.com
Jianmin Si, email: firstname.lastname@example.org
Keywords: long noncoding RNA; MTM; cell invasion; MT1F; gastric cancer
Received: September 07, 2016 Accepted: August 09, 2017 Published: October 26, 2017
The role of long non-coding RNAs (lncRNA) on gastric cancer (GC) are an emerging field. Here, we focused on a cancer-related lncRNA MTM and tried to explore its correlation with the development of GC. The expression of MTM was detected by qRT-PCR in GC cell lines and tissues. The relationship between MTM level and clinicopathological factors was then analyzed. Cell biological assays with overexpression or co-transfection approaches were examined to probe the functional relevance of this lncRNA and its potential targets. The results showed that MTM expression was significantly lower in GC cell lines and tissues, and closely correlated with lymphatic metastasis, invasive depth, tumor staging and overall survival. Overexpression of MTM significantly inhibited GC cell migration and invasion, suppressed cell proliferation and induced cell apoptosis. In addition, we found a positive correlation between the expression level of MTM and MT1F both in cell and tissue samples. MT1F overexpression decreased GC cell migration and invasion, while knockdown of MT1F restored cell migration and invasion in MTM-overexpressing GC cells, suggesting MT1F as a key target of MTM. Conclusively, abnormal decreased expression of MTM was observed in human GC, which might contribute to gastric carcinogenesis by modulating MT1F expression.
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