SOD2 (MnSOD) does not suppress tumorigenicity or metastasis of human melanoma C8161 cells.
Manganese superoxide dismutase (MnSOD, encoded by the SOD2 gene mapping to chromosome 6q25) has been implicated as a tumor suppressor and as a metastasis suppressor in some tumor cell lines. We showed that introduction of an intact chromosome 6 into the metastatic melanoma cell line C8161 completely suppressed metastasis but did not affect tumorigenicity (Welch et al., (1994) Oncogene 9:255). The purpose of this study was to test whether SOD2 is the gene responsible for metastasis suppression. MnSOD protein levels of C8161 (measured by Western blot), before and after transfer of chromosome 6, showed no correlation with metastatic potential. To determine whether the lack of correlation was due to mutant, nonfunctional SOD2, a highly metastatic subclone of C8161 (C8161c1.9) was transfected with functional SOD2 or vector control (pSFFV). Metastatic potential and tumorigenicity were unchanged. Southern and Northern blots confirmed the presence of the transfected SOD2; however, total MnSOD protein and antioxidant activity were not significantly altered. These results suggest that levels of MnSOD are highly regulated within C8161 melanoma cells and that SOD2 does not suppress tumor formation nor metastatic potential in all human melanomas.
Miele
M E
ME
Department of Pathology, Pennsylvania State University College of Medicine, M.S. Hershey Medical Center 17033-0850, USA.
McGary
C T
CT
Welch
D R
DR
D000818:Animals; D005260:Female; D006801:Humans; D008545:Melanoma / Q000517:prevention & control* / Q000556:secondary*; D051379:Mice; D008819:Mice, Nude; D012333:RNA, Messenger / Q000032:analysis; D013482:Superoxide Dismutase / Q000235:genetics / Q000502:physiology*; D014162:Transfection; D014407:Tumor Cells, Cultured
D012333:RNA, Messenger; D013482:Superoxide Dismutase