Posttranscriptional mechanisms are responsible for accumulation of truncated c-myc RNAs in murine plasma cell tumors

Abstract

c-myc Messenger RNAs are known to be extremely unstable (t1/2 = 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c-myc mRNAs in three murine plasmacytomas, where the c-myc gene either remains intact (ABPC20) or exists in a truncated form (MPC-11 and J558L) subsequent to 6;15 or 12;15 chromosome translocations respectively, and in an A-MuLV-induced pre-B lymphoma line (18-81.5) that lacks chromosome translocations and contains both c-myc genes in their normal context. The truncated myc genes in J558L and MPC-11 lack the promoters of the normal gene but are transcribed from cryptic promoters within the first c-myc intron. We found that posttranscriptional processes are largely responsible for the higher steady state accumulations of truncated c-myc transcripts, while broken and intact c-myc genes are transcribed at comparable rates.