6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Reduced tumor incidence, metastatic potential, and cytokine responsiveness of nm3-transfected melanoma cells

      , , , , , ,
      Cell
      Elsevier BV

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Reduced expression of the nm23 gene in certain rodent model systems and human breast tumors has been correlated with high tumor metastatic potential. To investigate the functional effects of nm23 expression, we have transfected a constitutive murine nm23-1 expression construct into highly metastatic K-1735 TK murine melanoma cells. TK clones expressing the exogenous nm23-1 construct exhibited a reduced incidence of primary tumor formation, significant reductions in tumor metastatic potential independent of tumor cell growth, and altered responses to the cytokine transforming growth factor beta 1 in soft agar colonization assays, compared with control-transfected TK clones. In contrast, nm23-1-transfected TK clones exhibited no significant differences in intrinsic tumor cell growth, i.e., primary tumor size in vivo, anchorage-dependent growth rate in vitro, and anchorage-independent colony formation in soft agar in vitro. The data demonstrate a suppressive effect of nm23 on several aspects of the cancer process, including tumor metastasis.

          Related collections

          Author and article information

          Journal
          Cell
          Cell
          Elsevier BV
          00928674
          April 1991
          April 1991
          : 65
          : 1
          : 25-35
          Article
          10.1016/0092-8674(91)90404-M
          2013093
          02a2229e-930b-4a9d-af95-d75f3957cb38
          © 1991

          https://www.elsevier.com/tdm/userlicense/1.0/

          History

          Comments

          Comment on this article