Yu Miaomiao, Sun Jiaying, Thakur Chitra, Chen Bailing, Lu Yongju, Zhao Hongwen, Chen Fei
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy, Wayne State University, Detroit, Michigan, United States of America ; Department of Pulmonary Medicine, Institute of Respiratory Diseases, The First Hospital of China Medical University, Shenyang, China ; Liaoning Cancer Hospital and Institute, Shenyang, China.
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy, Wayne State University, Detroit, Michigan, United States of America ; Department of Pulmonary Medicine, Institute of Respiratory Diseases, The First Hospital of China Medical University, Shenyang, China ; Respiratory Medicine, The 4th Affiliated Hospital, China Medical University, China.
PLoS One. 2014 Feb 4;9(2):e87998. doi: 10.1371/journal.pone.0087998. eCollection 2014.
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.
在多种人类癌症中均观察到矿物粉尘诱导基因(mdig,也称为mina53、MINA或NO52)的表达增加。mdig如何促进癌症发病机制的具体机制仍有待充分阐明。在本报告中,我们证明mdig的过表达降低了4',6-二脒基-2-苯基吲哚(DAPI)的核染色信号,同时细胞增殖显著增强。用shRNA沉默mdig导致细胞增殖在统计学上显著降低。有趣的是,mdig过表达降低了细胞在体外迁移和侵袭的能力,而用shRNA/siRNA沉默mdig则增强了迁移和侵袭能力。在临床上,我们发现癌症组织中mdig表达增加与肺癌患者较差的总生存率相关,尤其是对于那些无淋巴结转移的患者。综上所述,我们的结果表明mdig在细胞生长和运动性方面发挥相反的作用,这可能表明mdig在致癌作用的不同阶段具有矛盾的效应。