ZNF224 is a KRAB-zinc finger transcription factor that exerts a key tumor suppressive role in chronic myelogenous leukemia.

In this study, we identify the receptor tyrosine kinase Axl as a novel target of ZNF224 transcriptional repression activity. Axl overexpression is found in many types of cancer and is frequently associated with drug resistance. Interestingly, we also found that sensitivity to imatinib can be partly restored in imatinib-resistant chronic myelogenous leukemia cells by ZNF224 overexpression and the resulting suppression of Axl expression.

These results, in accordance with our previous findings, support the role of ZNF224 in imatinib responsiveness and shed new insights into potential therapeutic use of ZNF224 in imatinib-resistant chronic myelogenous leukemia.

ZNF224 是一种 KRAB-锌指转录因子，在慢性粒细胞白血病中发挥关键的肿瘤抑制作用。

在这项研究中，我们将受体酪氨酸激酶 Axl 鉴定为 ZNF224 转录抑制活性的新靶标。Axl 过度表达存在于许多类型的癌症中，并且通常与耐药性有关。有趣的是，我们还发现，通过 ZNF224 过表达和由此产生的 Axl 表达抑制，可以在伊马替尼耐药的慢性粒细胞白血病细胞中部分恢复对伊马替尼的敏感性。

根据我们之前的研究结果，这些结果支持 ZNF224 在伊马替尼反应性中的作用，并为 ZNF224 在伊马替尼耐药的慢性粒细胞白血病中的潜在治疗用途提供了新的见解。