Transcriptionally active RNA polymerases from Morris hepatomas and rat liver. Elucidation of the mechanism for the preferential increase in the tumour RNA polymerase I

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Abstract
The amount and/or activity of DNA-dependent RNA polymerases I, II and III from resting liver, regenerating liver and a series of Morris hepatomas (5123D, 7800, 7777, 3924A) were determined after extraction of the enzymes from whole tissue homogenates and subsequent fractionation by DEAE-Sephadex column chromatography. When compared with resting liver, the tumors exhibited a characteristic enzyme pattern in which polymerase I, but not II, was icreased. The increase in RNA polymerase I was proportional to the tumor growth rates. Alterations in polymerase III were confined to the most rapidly proliferating hepatomas. All classes of RNA polymerase were increased during liver regeneration. Relative to resting liver, the fastest growing tumor, 3924A, exhibited the highest activities and/or amounts of RNA polymerase I (8-fold) and III (5-fold)/g of tissue. These alterations in the tumor RNA polymerases were reflected in corresponding increases in the transcriptionally active (bound or chromatin-associated) enzyme population. The mechanisms underlying the augmented synthesis of RNA in vitro by bound polymerase I from hepatoma 3924A were elucidated by product analysis. Relative to liver RNA polymerase I, the tumor enzyme apparently produced more nascent RNA chains and elongated these chains at a faster rate. The number of 3''-termini, as measured by incorporation into uridine, was higher in the hepatoma even under conditions which prevented reinitiation, suggesting increased amount of transcriptionally active RNA polymerase I in the tumor.

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