Post-transcriptional regulation of messenger abundance in rat liver and hepatoma.

Saturation hybridisation with labelled single-copy DNA shows that polysomal poly(A)+ RNA of rat liver and of a minimum-deviation rat hepatoma cell-line (HTC) have similar total complexities and that few sequences are specific to either cell-type. Hybridisation kinetics of polysomal cDNAs with template and heterologous cell RNAs indicate that a proportion of liver messengers are at greatly reduced abundance in the hepatoma, but not the converse. Hybridisations using fractionated cDNAs enriched for abundant polysomal sequences confirm these findings: on average, abundant liver mRNAs are about 100-fold rarer in hepatoma, whereas abundant hepatoma mRNAs are only 5-fold rarer in liver. This pattern is also implied by cell-free translation of polysomal poly(A)+ RNAs. The reactions of total and fractionated polysomal cDNA probes with poly(A)+ nuclear RNA indicate that there is much less disparity in abundance of these sequences at nuclear level, implying that the differences arise, at least in part, post-transcriptionally. We interpret the altered mRNA abundances in the hepatoma in terms both of its decreased functional specialisation and its ability to proliferate.