Two discrete events, human T-cell leukemia virus type I tax oncoprotein expression and a separate stress stimulus, are required for induction of apoptosis in T-cells

被引：19

作者：

Kasaif T. ^{[1
]}

Jeang K.-T. ^{[1
]}

机构：

[1] Laboratory of Molecular Microbiology, NIAID, National Institutes of Health, Bethesda

来源：

Retrovirology | / 1卷 / 1期

关键词：

Jurkat Cell; Metallothionein Promoter; Oncoprotein Expression; Hct116 Colon Carcinoma Cell; Accelerate Cell Cycle Progression;

D O I：

10.1186/1742-4690-1-7

中图分类号：

学科分类号：

摘要：

Background. It is poorly understood why many transforming proteins reportedly enhance both cell growth (transformation) and cell death (apoptosis). At first glance, the ability to transform and the ability to engender apoptosis seem to be contradictory. Interestingly, both abilities have been widely reported in the literature for the HTLV-I Tax protein. Results. To reconcile these apparently divergent findings, we sought to understand how Tax might cause apoptosis in a Jurkat T-cell line, JPX-9. Tax expression can be induced equally by either cadmium (Cd) or zinc (Zn) in JPX-9 cells. Surprisingly, when induced by Zn, but not when induced by Cd, Tax-expression produced significant apoptosis. Under our experimental conditions, Zn but not Cd, induced SAPK (stress activated protein kinase)/JNK (Jun kinase) activation in cells. We further showed that transient over-expression of Tax-alone or Jun-alone did not induce cell death. On the other hand, co-expression of Tax plus Jun did effectively result in apoptosis. Conclusion. We propose that Tax-expression alone in a T-cell background insufficiently accounts for apoptosis. On the other hand, Tax plus activation of a stress kinase can induce cell death. Thus, HTLV-I infection/transformation of cells requires two discrete events (i.e. oncoprotein expression and stress) to produce apoptosis. © 2004 Kasai and Jeang; licensee BioMed Central Ltd.

引用

页数：12

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