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Tumor Promoter-induced Adhesion of the DS19 Clone of Murine Erythroleukemia Cells¹

Cancer Center/Institute of Cancer Research [H. Y., I. B. W., E. F., R. A. R., P. A. M.], Division of Environmental Sciences [H. Y., I. B. W.], and Departments of Medicine [I. B. W., R. A. R., P. A. M.] and Human Genetics and Development [R. A. R., P. A. M.], College of Physicians and Surgeons, Columbia University, New York, New York 10032

The potent mouse skin tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) causes the adhesion of suspension cultures of the DS19 clone of murine erythroleukemia cells (MELC) to the surface of tissue culture flasks. TPA-induced adhesion of MELC is apparent within 20 min and is maximum within 45 min after the addition of TPA to the culture. The effect requires as little TPA as 1 to 5 ng/ml. The adhesion is temperature dependent but is not inhibited by actinomycin D or cycloheximide. Partial inhibition is observed by colchicine and cytochalasin B. Among 6 phorbol esters and other plant diterpenes tested, there is a good correlation between effectiveness in inducing MELC adhesion and mouse skin tumor-promoting activity. TPA-induced adhesion is not seen when MELC are grown in bacterial flasks, yet differentiation is inhibited under these conditions, indicating that TPA-induced adhesion is not a prerequisite for TPA inhibition of differentiation. Two subclones of DS19 which are resistant to TPA-induced inhibition of differentiation show no adhesion to tissue culture flasks in the presence of TPA or other phorbol ester tumor promoters. When TPA-sensitive and -resistant cells are cocultured and TPA is added, almost all of the TPA-sensitive cells become adhesive to the plate, yet very few of the TPA-resistant cells become adhesive. Taken together, these results suggest that an early site of action of TPA in MELC is the cell surface membrane. The changes in MELC adhesion induced by TPA may provide clues to its mechanism of action and provide a rapid in vitro assay for certain types of tumor promoters.

¹ These studies were supported in part by grants and contracts from the National Cancer Institute (CA-13696, CA-18314, CA-21111, NO-1-CP-1008, and NO-1-CP-2-3234), the National Science Foundation (PCM-75-08696) and the American Cancer Society (CH-68). Part of this work was presented at the 17th Annual Meeting of the American Society for Cell Biology (30).

² Present address: Unit of Chemical Carcinogenesis, International Agency for Research on Cancer, 150, Cours Albert-Thomas-69372, Lyon, France.

³ Present address: Hematology Research Unit, Hebrew University, Hadassah Medical Center, Mt. Scopus, Israel.

Received 12/13/78. Accepted 3/ 9/79.