Abstract

The Ramos-Burkitt lymphoma (BL) B cell line is driven into growth arrest and apoptosis by cross-linking surface immunoglobulin. We demonstrate that protein kinase C (PKC) activity is required for Ramos B cell proliferation and survival. A variety of PKC inhibitors trigger a significant decrease in [3H]thymidine incorporation with a concomitant increase in cell death. Antisense depletion of expression of the PKC-α isoform is sufficient to trigger cell death in the absence of any other signal, demonstrating a requirement for this isoform for survival of Ramos-BL B cells. Cross-linking surface immunoglobulin also leads to depletion of PKC-α levels, suggesting that this may be one mechanism by which this signals for cell death in Ramos-BL B cells.

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