PT  - JOURNAL ARTICLE
AU  - Frisch, Steven M.
AU  - Dolter, Karen E.
TI  - Adenovirus <em>Ela</em>-mediated Tumor Suppression by a c-<em>erb</em>B-2/<em>neu</em>-independent Mechanism
DP  - 1995 Dec 01
TA  - Cancer Research
PG  - 5551--5555
VI  - 55
IP  - 23
4099  - http://cancerres.aacrjournals.org/content/55/23/5551.short
4100  - http://cancerres.aacrjournals.org/content/55/23/5551.full
SO  - Cancer Res1995 Dec 01; 55
AB  - We reported previously that the adenovirus E1a gene reversed the transformed phenotype of one human melanoma and one fibrosarcoma cell line (S. Frisch, Proc. Natl. Acad. Sci. USA, 88: 9077–9081, 1991). To determine the generality of the tumor suppression effects of E1a, a diversity of tumor cell lines, including A204 rhabdomyosarcoma, RD rhabdomyosarcoma, Saos-2 osteosarcoma, NCI-H23 non-small cell lung carcinoma, MDA-MB435S breast carcinoma, and ras-transformed MDCK kidney epithelial cells, were infected with a retrovirus bearing the 12S E1a coding sequence. We demonstrate here that the expression of E1a severely reduced the anchorage-independent and tumorigenic growth of these cell lines without affecting their growth under normal culture conditions. The parental tumor cells used in this study did not overexpress c-erbB-2/neu, and E1a did not affect its expression in these cells. Thus, tumor suppression by E1a can operate in a wide variety of human tumor cells by c-erbB-2/neu-independent mechanisms. E1a also sensitized these cell lines to the cytotoxic effects of the anticancer drugs etoposide and cisplatin. The results suggest that E1a could prove useful for the gene therapy of a wide variety of human cancers. ©1995 American Association for Cancer Research.