4.7 Article

Nme1andNme2genes exert metastasis-suppressor activities in a genetically engineered mouse model of UV-induced melanoma

Journal

BRITISH JOURNAL OF CANCER
Volume 124, Issue 1, Pages 161-165

Publisher

SPRINGERNATURE
DOI: 10.1038/s41416-020-01096-w

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Funding

  1. National Institutes of Health/National Cancer Institute [CA83237, CA159871, CA159871-S1]
  2. National Institutes of Health/National Institute of General Medical Sciences [T32 CA154274, R25 GM055036]
  3. NIH Intramural Research Program
  4. Merit Award from the Department of Veterans Affairs [1I01BX004293-01A1]
  5. Maryland Stem Cell Research Foundation [MSCRFI-1638]

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NME1 and NME2 genes have a significant impact on metastatic activity in a mouse model of melanoma, with NME2 showing MSG activity for the first time in a spontaneous cancer model, and NME1 displaying a novel metastasis-suppressor function in UVR-induced melanoma.
NME1is a metastasis-suppressor gene (MSG), capable of suppressing metastatic activity in cell lines of melanoma, breast carcinoma and other cancer origins without affecting their growth in culture or as primary tumours. Herein, we selectively ablated the tandemly arrangedNme1andNme2genes to assess their individual impacts on metastatic activity in a mouse model (HGF:p16(-/-)) of ultraviolet radiation (UVR)-induced melanoma. Metastatic activity was strongly enhanced in both genders ofNme1-andNme2-null mice, with stronger activity in females across all genotypes. The study ascribes MSG activity toNme2for the first time in an in vivo model of spontaneous cancer, as well as a novel metastasis-suppressor function toNme1in the specific context of UVR-induced melanoma.

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