Paradoxical roles of mineral dust induced gene on cell proliferation and migration/invasion
Miaomiao Yu1, Jiaying Sun2, Chitra Thakur3
1Department 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.
Abstract:
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.
Insights
Mineral dust-induced gene (mdig) overexpression enhances cancer cell proliferation but reduces migration. Increased mdig expression in lung cancer correlates with poorer survival, suggesting a paradoxical role in carcinogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Gene Expression
Background:
- Increased expression of mineral dust-induced gene (mdig) is observed in human cancers.
- The precise role of mdig in cancer pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the functional role of mdig in cancer cell proliferation, migration, and invasion.
- To correlate mdig expression with clinical outcomes in lung cancer patients.
Main Methods:
- Overexpression and silencing (shRNA/siRNA) of mdig in cancer cells.
- Assessment of cell proliferation, nuclear morphology (DAPI staining), migration, and invasion.
- Analysis of mdig expression in lung cancer tissues and correlation with patient survival data.
Main Results:
- Mdig overexpression decreased DAPI nuclear staining and enhanced cell proliferation.
- Silencing mdig significantly decreased cell proliferation.
- Mdig overexpression reduced cell migration and invasion, while silencing enhanced these processes.
- Increased mdig expression in lung cancer tissues correlated with poorer overall survival, particularly in patients without lymph node metastasis.
Conclusions:
- Mdig exhibits opposing effects on cancer cell growth and motility.
- These findings suggest a paradoxical role for mdig in different stages of carcinogenesis.
- Mdig may serve as a potential prognostic biomarker in lung cancer.
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