DNA replication initiation is a tightly controlled process in normal cells to ensure the faithfulness and accuracy of DNA replication. In contrast, aberrant expression of DNA replication-initiation proteins results in deregulated cell proliferation in cancer cells. However, the mechanisms that modulate expression of DNA replication-initiation proteins in normal and cancer cells are still largely unclear. miRNAs, most of which are downregulated in cancer, might be one of possible mechanisms that regulate DNA replication-initiation proteins. In this study, we demonstrate that miR-495-3p and miR-370-3p repress DNA replication licensing, cell proliferation in vitro and in vivo by targeting MCM2. Besides, clinical evidence shows that expressions of miR-495-3p and miR-370-3p are signi...[ Read more ]

DNA replication initiation is a tightly controlled process in normal cells to ensure the faithfulness and accuracy of DNA replication. In contrast, aberrant expression of DNA replication-initiation proteins results in deregulated cell proliferation in cancer cells. However, the mechanisms that modulate expression of DNA replication-initiation proteins in normal and cancer cells are still largely unclear. miRNAs, most of which are downregulated in cancer, might be one of possible mechanisms that regulate DNA replication-initiation proteins. In this study, we demonstrate that miR-495-3p and miR-370-3p repress DNA replication licensing, cell proliferation in vitro and in vivo by targeting MCM2. Besides, clinical evidence shows that expressions of miR-495-3p and miR-370-3p are significantly decreased, while MCM2 is upregulated in human stomach cancer tissues compared with the adjacent normal tissues. These data suggest that miR-495-3p and miR-370-3p function as tumor suppressors by targeting MCM2 in cancer, and these findings may provide clues for cancer detection and therapy.

Lung cancer is a deadly disease due to metastasis in late stages. To investigate the mechanisms of metastasis in lung cancer, we identified a CEP72 mutation in lung cancer metastatic lymph nodes by whole exosome sequencing. We found that CEP72 is needed for mitosis, migration and invasion of lung cancer cells. Importantly, cell polarity and branched F-actin formation are impaired in CEP72-depleted cells, suggesting that CEP72 is involved in the migration and invasion of lung cancer cells by promoting F-actin formation.