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Published on: January 24, 2016

Interferon-induced modulation of human ras oncogene expression

D Samid, Z Schaff, E H Chang

    Progress in Clinical and Biological Research
    |January 1, 1985
    PubMed

    Insights

    Interferon (IFN) treatment reversed ras oncogene-induced cell transformation. This resulted in reverted tumor cells with normal morphology and growth, demonstrating reduced oncogene expression.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Cell Biology

    Background:

    • Cell transformation by oncogenes like c-Ha-ras1 drives cancer development.
    • Interferon (IFN) is known for its anti-proliferative and anti-viral effects.
    • Understanding how IFN impacts oncogene expression is crucial for cancer therapy.

    Purpose of the Study:

    • To investigate the effect of interferon (IFN) on ras oncogene-induced cell transformation.
    • To analyze the impact of IFN on oncogene expression in established tumor cells.

    Main Methods:

    • NIH 3T3 cells were transfected with human bladder carcinoma c-Ha-ras1 oncogene DNA.
    • Transfected cells and an established tumor line (RS485) were treated with IFN.
    • Phenotypic reversion, cell morphology, growth characteristics, soft agar colony formation, and tumorigenicity in nude mice were assessed.
    • Levels of c-Ha-ras1 mRNA and the onc-encoded protein p21 were quantified.

    Main Results:

    • IFN treatment inhibited ras-induced cell transformation in NIH 3T3 cells.
    • IFN treatment of RS485 tumor cells led to the emergence of reverted colonies with normal morphology and growth.
    • Revertant cells exhibited contact inhibition, failed to grow in soft agar, and were non-tumorigenic in nude mice.
    • Revertant cells showed significantly decreased levels of c-Ha-ras1 mRNA and p21 protein compared to parental RS485 cells, despite retaining the transfected oncogene.

    Conclusions:

    • Interferon (IFN) can reverse oncogene-induced cell transformation and suppress the malignant phenotype.
    • IFN treatment downregulates the expression of the c-Ha-ras1 oncogene and its encoded protein p21.
    • These findings suggest a potential therapeutic role for IFN in cancers driven by ras oncogene activation.

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