Paradoxical roles of mineral dust induced gene on cell proliferation and migration/invasion

• Published in: PloS one Vol. 9; no. 2; p. e87998
• Main Authors: Yu, Miaomiao, Sun, Jiaying, Thakur, Chitra, Chen, Bailing, Lu, Yongju, Zhao, Hongwen, Chen, Fei
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 04.02.2014; Public Library of Science (PLoS)
• Subjects: B cells; Biology; Breast cancer; Cancer; Cancer metastasis; Carcinogenesis; Carcinogens; Cell cycle; Cell growth; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell Proliferation; Colorectal cancer; Development and progression; Dioxygenases; Dust; Esophagus; Gene expression; Gene Expression Regulation, Neoplastic - genetics; Genes; Histone Demethylases; Hospitals; Humans; Liver cancer; Lung cancer; Lung diseases; Lung Neoplasms - genetics; Lymph nodes; Lymphoma; Medical prognosis; Medicine; Metastases; Neoplasm Invasiveness - genetics; Neuroblastoma; Nuclear Proteins - genetics; Pathogenesis; Pharmaceutical sciences; Pharmacy; Physics; Proteins; Respiratory diseases; RNA, Small Interfering - genetics; siRNA; Statistical analysis; Survival analysis; Tissues
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0087998

Increased expression of mineral dust-induced gene (mdig, also named as mina53, MINA, or NO52) has been observed in a number of human cancers. The mechanism of how mdig contribute to the pathogenesis of cancer remains to be fully elucidated. In this report, we demonstrated that overexpression of mdig decreased the nuclear staining signal by 4',6-diamidino-2-phenylindole (DAPI), along with a considerable enhancement in cell proliferation. Silencing mdig by shRNA resulted in a statistically significant decrease of cell proliferation. Intriguingly, mdig overexpression reduced the capacity of the cells in migration and invasion in vitro, whereas silencing mdig by shRNA/siRNA enhanced migration and invasion. Clinically, we found that increased expression of mdig in cancer tissues correlates with poorer overall survival of the lung cancer patients, esp., for those without lymph node metastasis. Taken together, our results suggest that mdig plays opposite roles on cell growth and motility, which possibly indicates the paradoxical effect of mdig at the different stages of carcinogenesis.