Research SummarySenior Fellowship research summary
Anti-metastatic function of Non Metastatic 2 (NME2) has been demonstrated in human cancers; however mechanisms of metastases control by NME2 are poorly understood. In this context, recent observations implicating the involvement of chromosome-ends (telomeres) in metastatic outcome are interesting. Notably, though it is well-established that telomere dysfunction causes tumor growth, involvement of telomeres in metastasis progression is poorly understood. Recent data from our laboratory may help understand the emerging role of telomeres in metastases. While investigating the mechanisms underlying metastasis control by NME2, we found that it localizes at telomere ends and interacts with telomere binding factors. These findings present a novel opportunity to investigate telomere related interactions in the context of NME2-mediated metastasis suppression. Results are expected to help understand the mechanisms of metastases control from a new angle.
Increase in focal adhesion (focal adhesion factor vinculin stained in red) was found in human fibrosarcoma-derived cells expressing low levels of the metastases suppressor Non-Metastatic 2 (NME2). Cells were co-stained using Phalloidin alexa fluor 488.