Overexpression of xCT induces up-regulation of 14-3-3beta in Kaposi's sarcoma.
Overexpression of xCT induces up-regulation of 14-3-3beta in Kaposi's sarcoma.
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DOI：
10.1042/bsr20090163
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发表时间：
2010-03-25
影响因子：
4
通讯作者：
Li W
中科院分区：
文献类型：
--
作者：
Zeng Y;Li Y;Chen RS;He X;Yang L;Li W
KSHV（卡波西肉瘤相关疱疹病毒）或HHV-8（人类疱疹病毒8）与KS的发病机制有关，KS是最常见的艾滋病相关恶性肿瘤。xCT（胱氨酸/谷氨酸转运体xc -系统的功能亚基）被称为HHV-8融合进入受体，也是一种致癌蛋白。xCT如何触发HHV-8感染的信号转导和细胞增殖尚不清楚。我们发现xCT在KS组织和hhv -8阳性BCBL-1细胞中过表达。将xCT cDNA质粒转染到hhv -8阴性的BJAB细胞中，14-3-3β表达增加，细胞生长速度加快。相比之下，xCT siRNA（短干扰RNA）或xCT抑制剂磺胺嘧啶均能抑制hhv -8阳性BCBL-1细胞14-3-3β的表达和细胞生长速度。这些结果表明14-3-3β是xCT在KS中介导细胞增殖的下游效应因子。
KSHV (Kaposi's sarcoma-associated herpesvirus), or HHV-8 (human herpesvirus 8), is associated with the pathogenesis of KS, the most common AIDS-related malignancy. xCT (functional subunit of the cystine/glutamate transporter xc− system) is known as the HHV-8 fusion-entry receptor as well as an oncogenic protein. How the xCT triggers the signal transduction of HHV-8 infection and the cell proliferation remains incomplete. We found that xCT was overexpressed in KS tissues and HHV-8-positive BCBL-1 cells. When xCT cDNA plasmids were transfected into the HHV-8-negative BJAB cells, the expression of 14-3-3β and cell growth rate were increased. In contrast, the expression of 14-3-3β and the cell growth rate of HHV-8-positive BCBL-1 cells were suppressed by either xCT siRNA (short interfering RNA) or an xCT inhibitor, sulfsalazine. These results suggest that 14-3-3β is a downstream effector of xCT in KS to mediate the cell proliferation.