Tumor induction by the c-Myc target genes rcl and lactate dehydrogenase A

B. C. Lewis, J. E. Prescott, S. E. Campbell, H. Shim, R. Z. Orlowski, C. V. Dang

Research output: Contribution to journalArticlepeer-review

Abstract

The characterization of c-Myc target genes, such as rcl and lactate dehydrogenase A (LDH-A), is critical for understanding the mechanisms of c-Myc-induced cell transformation and tumorigenesis. We have previously demonstrated that Rcl induces anchorage-independent growth in Rat1a fibroblasts and that LDH-A is required for cell transformation by c-Myc. In this study, we report that Rcl and LDH-A act synergistically to induce anchorage-independent growth. Cells expressing both Rcl and LDH-A form tumors after s.c. injection into nude mice, although neither Rcl or LDH-A overexpression alone induces tumorigenesis. The inability of Rcl and LDH-A to fully recapitulate c-Myc activity, however, indicates that other c-Myc target genes participate in tumorigenesis. In addition, cells that coexpress Rcl and vascular endothelial growth factor are more comparable with c-Myc overexpressing cells in their ability to form tumors in nude mice. These findings confirm Rcl and LDH-A as critical components of the cell transformation program induced by c-Myc and suggest that Rcl is tumorigenic in cells that are provided with a permissive metabolic milieu.

Original languageEnglish (US)
Pages (from-to)6178-6183
Number of pages6
JournalCancer Research
Volume60
Issue number21
StatePublished - Nov 1 2000

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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