In uveal melanoma (UM) cells, the protein kinase C (pathway) is almost generally constitutively activated as a result of an activating mutation in either the GNAQ or the GNA11 G-protein. A pan-PKC inhibitor, sotrastaurin (also named AEB071), is in clinical trials for treatment of UM patients with limited success and eliciting adverse effects. Interestingly, genetic interference with expression of just one PKC isoform, e.g., PKCδ, is sufficient to reduce UM cell proliferation. Therefore, we tested the effect of a recently described specific PKCδ inhibitor, B106, on growth and survival of UM cell lines. Surprisingly, we found that B106 efficiently induced apoptosis in several cell lines, but apparently independent of activated PKCδ.

中文翻译：

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选择性PKCδ抑制剂B106引起葡萄膜黑色素瘤的生长抑制作用，而与活化的PKC同工型无关。

在葡萄膜黑色素瘤（UM）细胞中，由于GNAQ或GNA11 G蛋白的激活突变，蛋白激酶C（途径）几乎通常被组成性激活。泛PKC抑制剂sotrastaurin（也称为AEB071）正在临床试验中，用于治疗成功率有限且引起不良反应的UM患者。有趣的是，仅表达一种PKC同工型，例如PKCδ的遗传干扰足以减少UM细胞增殖。因此，我们测试了最近描述的特定PKCδ抑制剂B106对UM细胞系生长和存活的影响。出人意料的是，我们发现B106有效诱导了几种细胞系的凋亡，但显然不依赖于活化的PKCδ。