Perkins A, Kongsuwan K, Visvader J, Adams J M, Cory S
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Proc Natl Acad Sci U S A. 1990 Nov;87(21):8398-402. doi: 10.1073/pnas.87.21.8398.
In the murine myelomonocytic leukemia WEHI-3B, proviral insertions have induced expression of the Hox-2.4 homeobox gene and the gene for the myeloid growth factor interleukin 3 (IL-3). To assess their potential oncogenic role, normal bone marrow cells were infected with retroviruses bearing the genes for IL-3 or IL-3 plus Hox-2.4. Unlike the IL-3 virus, the IL-3/Hox-2.4 virus was highly leukemogenic. Infected cells expressing both genes exhibited retarded differentiation in vitro, generated myelomonocytic cell lines, and provoked a rapid, transplantable myeloid leukemia in vivo. The oncogenic action of Hox-2.4 appears to derive from its ability to impede the IL-3-driven terminal differentiation of myeloid cells. The results suggest that homeobox genes can regulate key differentiation processes such as self-renewal capacity and that their inappropriate expression can be oncogenic.
在鼠骨髓单核细胞白血病WEHI-3B中,前病毒插入已诱导同源框基因Hox-2.4以及髓系生长因子白细胞介素3(IL-3)基因的表达。为评估它们潜在的致癌作用,用携带IL-3基因或IL-3加Hox-2.4基因的逆转录病毒感染正常骨髓细胞。与IL-3病毒不同,IL-3/Hox-2.4病毒具有高度致白血病性。表达这两种基因的感染细胞在体外表现出分化延迟,产生了骨髓单核细胞系,并在体内引发了快速的、可移植的髓系白血病。Hox-2.4的致癌作用似乎源于其阻碍IL-3驱动的髓系细胞终末分化的能力。结果表明,同源框基因可调节关键的分化过程,如自我更新能力,且其异常表达可能具有致癌性。