A variant form of ETS1 induces apoptosis in human colon cancer cells.

Abstract

We have previously shown that the human ETS1 protein (p51-ETS1), when ectopically expressed in colon cancer cell lines, is able to reduce its tumorigenicity without affecting its growth properties. To understand the mechanism of tumor reduction, we have expressed two different forms of ETS1 in colon cancer cell lines. Data presented in this paper indicate that the naturally occurring spliced variant protein, p42-ETS1, lacking the region encoded by ETS1 exon VII, represses the tumorigenicity, while p51-ETS1 reduces the tumorigenicity. Repression of tumorigenicity mediated by p42-ETS1 appears to be caused by its ability to induce apoptosis in epithelial cancer cells. This work can have profound medical significance in that it may open up new insights into the potential role of the p42-ETS1 in the induction of apoptosis in epithelial cell cancers and may provide a rationale for its use for potential gene therapy experiments to initiate cell death in cancer cells.

• Authors: C C Huang, T S Papas, N K Bhat
• Journal: Oncogene (Oncogene) Vol. 15 Issue 7 Pg. 851-6 (Aug 14 1997) ISSN: 0950-9232 [Print] England
• PMID: 9266972 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• ETS1 protein, human
• Ets1 protein, mouse
• Protein Synthesis Inhibitors
• Proto-Oncogene Protein c-ets-1
• Proto-Oncogene Proteins
• Proto-Oncogene Proteins c-ets
• Transcription Factors
• Tetracycline

Topics

• Animals
• Apoptosis (physiology)
• Cell Nucleus (metabolism)
• Colonic Neoplasms (metabolism, pathology, prevention & control)
• Humans
• Mice
• Mice, Nude
• Protein Synthesis Inhibitors (pharmacology)
• Proto-Oncogene Protein c-ets-1
• Proto-Oncogene Proteins (chemistry, drug effects, genetics, physiology)
• Proto-Oncogene Proteins c-ets
• Tetracycline (pharmacology)
• Transcription Factors (chemistry, drug effects, genetics, physiology)
• Transfection
• Tumor Cells, Cultured