It was found that protooncogene c-fos was over-expressing in SAC-IIB_2 cell strains. Targeting the code 2-7 sequence of c-fos cDNA of mice, we designed and synthesised eighteen mers antisense. sense and nonsense oligodeoxynucleotides(ODN). The results indicated that antisense c-fos ODN could induce SAC- IIB_2 maturative differentiation, inhibit its growth rate, decrease its ability of forming tumor in nude mice and expression of Fos protein, however, antisense ODN has no remarkable effect on cellular dynamics of SAC-IIB2. But sense and nonsense c-fos ODN have no similar effect on SAC-IIB_2 cell strains. The results demonstrated that antisense c-fos oligodeoxynucleotide has inhibition effects on malignant phenotype of mice SRS lymphoma cell.

AIM: To study the role of c-myc oncogene in L6565 leukemia oncogenesis and the effects of therapy by inhibition of its expression with antisense c-myc. METHODS: A recombinant retroviral vector containing antisense c-myc of the murine (pGNCas)was constructed and then transfected into PA317 cells by the method of calcium phosphate precipitation. L6565 clone cells were infected with retrovirus particles. Stable integretion of antisense c-myc was shown by PCR. The change of the malignance and phenotype of L6565as were detected by the examination of the growth, morphology, cells cycle, agar assay and expression of c-myc. RESULTS: The shape of most L6565as cells became spherical. The growth of L6565as was inhibited compared to control cells. The analysis of cells cycle: L6565as cells were arrest in G 0/G 1 phase, decreased in S phase. The ability of L6565as cells to form colony in soft agarose was significantly suppressed. c-myc in L6565as cells was lowly expressed. CONCLUSION: (1)c-myc plays a critical role in L6565 leukemia oncogenesis; (2)Inhibition of expression of c-myc makes partly reversion of malignant phenotype of L6565 murine leukemia clone cells.