Suppression of src-induced transformed phenotype by expression of tropomyosin-1

Oncogene. 1999 Mar 18;18(11):2027-31. doi: 10.1038/sj.onc.1202264.

Abstract

Suppression of high M(r) tropomyosins (TMs) is a common feature of transformed cells. Previous work from this laboratory has demonstrated that the isoform 1 of TM, TM1, acts as an anti-oncogene in ras-transformed murine fibroblasts. In this study, we have investigated whether TM1 is a ras-specific suppressor, or a general suppressor protein of the cellular transformation. V-src transformed fibroblasts, which express decreased TM1, were transduced with a full-length cDNA to overexpress TM1. Both the control and the transduced cells expressed v-src kinase at comparable levels. TM1 expressing (src-T1) cells grew at a lower rate in monolayer, exhibited well spread, flat morphology than the control cells. Enhanced expression of TM1 resulted in improved microfilamental architecture. More significantly, src-T1 cells completely failed to grow under anchorage independent conditions. These data demonstrate that TM1 is as an anti-oncogene of functionally diverse oncogenes, and it is a class II tumor suppressor protein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Division
  • Cell Transformation, Neoplastic*
  • Drosophila Proteins*
  • Mice
  • Oncogene Protein pp60(v-src) / genetics
  • Oncogene Protein pp60(v-src) / metabolism*
  • Phenotype
  • Tropomyosin / biosynthesis*
  • Tropomyosin / genetics

Substances

  • Drosophila Proteins
  • Tm2 protein, Drosophila
  • Tpm1 protein, mouse
  • Tropomyosin
  • Oncogene Protein pp60(v-src)