Inappropriate transcriptional repression involving histone deacetylases (HDACs) is a prominent cause for the development of leukemia. We now identify faulty expression of a specific mediator of transcriptional repression in a solid tumor. Loss of the adenomatosis polyposis coli (APC) tumor suppressor induces HDAC2 expression depending on the Wnt pathway and c-Myc. Increased HDAC2 expression is found in the majority of human colon cancer explants, as well as in intestinal mucosa and polyps of APC-deficient mice. HDAC2 is required for, and sufficient on its own to prevent, apoptosis of colonic cancer cells. Interference with HDAC2 by valproic acid largely diminishes adenoma formation in APC(min) mice. These findings point toward HDAC2 as a particularly relevant potential target in cancer therapy.

中文翻译：

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在结肠直肠肿瘤发生中APC丢失后诱导HDAC2表达。

涉及组蛋白脱乙酰基酶（HDACs）的不适当的转录抑制是白血病发展的重要原因。我们现在确定实体肿瘤中转录抑制的特定介体的错误表达。取决于Wnt途径和c-Myc，腺瘤性息肉病大肠埃希氏菌（APC）肿瘤抑制剂的丧失诱导HDAC2表达。在大多数人类结肠癌外植体以及APC缺陷小鼠的肠粘膜和息肉中发现HDAC2表达增加。HDAC2是结肠癌细胞凋亡所必需的，并且其自身足以预防结肠癌细胞的凋亡。丙戊酸对HDAC2的干扰大大减少了APC（min）小鼠中腺瘤的形成。这些发现表明，HDAC2是癌症治疗中特别相关的潜在靶标。