Cycloheximide Increases Endogenous Retroviral RNA Levels in Murine Liver and Lung

The expression of moloney murine leukemia virus (Mo-MuLV), intracisternal A particle (IAP), virus-like 30S sequence (VL30), early transposon (ET) endogenous retroviral sequences was analysed in the liver of untreated C3Hf, C57BL/6J and AKR mice, and in the lungs of untreated A/J, BALB/c, C3Hf and C57BL/6J mice. C3Hf mice are genetically susceptible to hepatocarcinogenesis, whereas the other strains are resistant. A/J and BALB/c mice are genetically susceptible to lung carcinogenesis, whereas the other strains are resistant. Both in liver and lung tissues we found differences between murine strains in the pattern of basal retrovirus expression. The effect of inhibition of protein synthesis on the levels of retroviral mRNAs was studied in the same tissues and strains 3 h following in vivo cycloheximide treatment. Cycloheximide treatment increased the liver and lung levels of virus Mo-MuLV, IAP, ET related transcripts in a strain dependent way, whereas VL30 mRNA levels increased in both tissues of all strains examined. These results suggested the existence of labile proteins that regulate the abundance of specific retroviral mRNAs in murine liver and lung in a strain specific fashion. No clear relationships between pattern of retrovirus expression and genetical susceptibility to hepatocarcinogenesis was found. The strains genetically resistant to lung carcinogenesis (C3Hf, C57BL/6J) showed higher lung basal levels and higher cycloheximide inducibility of mRNAs homologous to Mo-MuLV than the susceptible strains (A/J, BALB/c).