Dean M, Cleveland J L, Rapp U R, Ihle J N
NCI-Frederick Cancer Research Facility, Program Resources, Inc., Maryland 21701.
Oncogene Res. 1987 Aug;1(3):279-96.
We have constructed a recombinant retrovirus containing the murine c-myc and the neo gene and introduced the virus into the interleukin-3 (IL3) dependent myeloid cell line FDC-P1. Unregulated expression of the introduced c-myc gene is associated with both an increased viability and constitutive ornithine decarboxylase mRNA levels in FDC-P1 cells grown in the absence of IL3. FDC-P1 cells infected with the c-myc virus gave rise to IL3 independent lines. Three out of four independent lines have an activated endogenous c-myc or N-myc gene. We have also shown that c-myc mRNA levels are tightly regulated by IL3 in FDC-P1 cells. Taken together these results indicate that myc plays a critical role in the signal transduction pathway of IL3. Furthermore, activation of the N-myc gene may be one mechanism for myeloid cells to progress to complete IL3 independence.
我们构建了一种包含鼠源c-myc和neo基因的重组逆转录病毒,并将该病毒导入依赖白细胞介素-3(IL3)的髓系细胞系FDC-P1。导入的c-myc基因的失控表达与在无IL3条件下生长的FDC-P1细胞中活力增加以及鸟氨酸脱羧酶mRNA水平的组成性表达相关。感染c-myc病毒的FDC-P1细胞产生了不依赖IL3的细胞系。四个独立细胞系中有三个具有激活的内源性c-myc或N-myc基因。我们还表明,在FDC-P1细胞中,c-myc mRNA水平受IL3严格调控。综合这些结果表明,myc在IL3的信号转导途径中起关键作用。此外,N-myc基因的激活可能是髓系细胞发展为完全不依赖IL3的一种机制。