Missing in metastasis B (MIM-B) has been widely reported to inhibit cancer cell invasion and proliferation in a variety of human cancers. However, the functions of MIM-B in lung cancers are still controversial. In addition, the mechanisms and regulation of MIM-B are poorly understood. In the present study, we found that the invasion level of 95C human lung giant-cell carcinoma cells was elevated when MIM-B was knocked down, while the invasion of 95D was suppressed when MIM-B was overexpressed, proving that MIM-B suppresses human lung giant-cell carcinoma cell invasion, which is similar to its function in most cancers. Furthermore, we reported that an increase in DNA methylation density in the promoter of MIM-B by DNA methyltransferase 1 (DNMT1) is correlated with the silencing of MIM-B expression and the high metastasis of 95D human lung giant-cell carcinoma cell line. Taken together, MIM-B, which is regulated by DNMT1 through DNA methylation, is a putative cancer suppressor in human lung giant-cell carcinoma.
CITATION STYLE
Wang, H., Yu, X., Wang, X., Li, X., & Yang, S. (2017). Missing in metastasis B, regulated by DNMT1, functions as a putative cancer suppressor in human lung giant-cell carcinoma. Acta Biochimica et Biophysica Sinica, 49(3), 238–245. https://doi.org/10.1093/abbs/gmw138
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