Oncogenic transformation by the tax gene of human T-cell leukemia virus type I in vitro

Journal Article · Thu Feb 01 04:00:00 EST 1990 · Proceedings of the National Academy of Sciences of the United States of America; (USA)

DOI:https://doi.org/10.1073/pnas.87.3.1071· OSTI ID:6699753

Tanaka, Atsushi; Takahashi, Chiaki; Yamaoka, Shoji; Nosaka, Tetsuya; Maki, Masatoshi; Hatanaka, Masakazu ^[1]

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1. Kyoto Univ. (Japan)

Human T-cell leukemia virus type I (HTLV-I) is a causative agent of adult T-cell leukemia (ATL). To elucidate the role of HTLV-I in leukemogenesis, the authors examined the biological activity of a defective HTLV-I provirus with the env-pX 3{prime} long terminal repeat region cloned from leukemic cells of an ATL patient. Transfection experiments showed growth stimulation of NIH 3T3 cells--growing beyond the saturation density and growing in soft agar. Since the pX sequence is known to encode three proteins, Tax, Rex, and p21{sup x}, the biological activity of each pX gene was examined separately. The growth-stimulating activity was induced only by the tax gene in NIH 3T3 cells and Rat-1 cells. Furthermore, the tax gene induced tumorigenicity in nude mice when introduced into Rat-1 cells. Thus, a transcriptional transactivator gene of HTLV-I, tax, is clearly identified as a viral oncogene without a cellular homolog. The transforming activity of tax, possibly via a transcriptional deregulation of cell growth control, may play an important role in leukemogenesis of ATL in addition to its aberrant stimulation of the interleukin 2 system.

• OSTI ID: 6699753
• Journal Information: Proceedings of the National Academy of Sciences of the United States of America; (USA), Journal Name: Proceedings of the National Academy of Sciences of the United States of America; (USA) Vol. 87:3; ISSN 0027-8424; ISSN PNASA
• Country of Publication: United States
• Language: English

Related Subjects

550201* -- Biochemistry-- Tracer Techniques
59 BASIC BIOLOGICAL SCIENCES
ANIMAL CELLS
CARCINOGENESIS
CELL CONSTITUENTS
CELL CULTURES
CELL TRANSFORMATIONS
CONNECTIVE TISSUE CELLS
DISEASES
ETIOLOGY
FIBROBLASTS
GENES
HEMIC DISEASES
IMMUNE SYSTEM DISEASES
LEUKEMIA
MICROORGANISMS
MORPHOLOGY
NEOPLASMS
ONCOGENIC TRANSFORMATIONS
ONCOGENIC VIRUSES
PARASITES
PATHOGENESIS
PATIENTS
PLASMIDS
SOMATIC CELLS
TRANSCRIPTION
TUMOR CELLS
VIRUSES