Cancer-testis (CT) antigens, rarely in normal tissues except testis, are expressed in many tumor types. In recent years, DDX43 has been shown to be expressed in several malignancies. However, the role of DDX43 during tumorigenesis is not well established. In the present study, we explored the function of DDX43 in chronic myeloid leukemia (CML). We found that DDX43 overexpression in CML cell lines enhanced survival and colony formation, inhibited cell apoptosis, promoted tumorigenesis, and CML progression. In contrast, silencing of DDX43 inhibited cell survival and tumorigenesis. Upregulated H19 and downregulated miR-186 were identified in DDX43-transfected cells. Furthermore, we demonstrated that miR-186 targeted DDX43, and overexpressed miR-186 increased apoptosis and decreased cell survival. We also showed that DDX43 regulated the expression of H19 through demethylation and silencing H19 inhibited cell survival. Taken together, these results indicate that DDX43 provides critical support to the progression of CML by enhancing cell survival, colony formation, and inhibiting cell apoptosis, thereby implicating DDX43 as a potential therapeutic target in CML.

中文翻译：

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DDX43抑制miR-186和释放H19有助于肿瘤发生和CML进展。

睾丸癌（CT）抗原在除睾丸以外的其他正常组织中很少表达，在许多类型的肿瘤中都有表达。近年来，已经证明DDX43在几种恶性肿瘤中表达。但是，DDX43在肿瘤发生过程中的作用尚不明确。在本研究中，我们探讨了DDX43在慢性粒细胞白血病（CML）中的功能。我们发现CML细胞系中DDX43的过表达增强了存活率和集落形成，抑制了细胞凋亡，促进了肿瘤的发生和CML的进展。相反，使DDX43沉默可抑制细胞存活和肿瘤发生。在DDX43转染的细胞中鉴定出上调的H19和下调的miR-186。此外，我们证明了miR-186靶向DDX43，而过表达的miR-186增加了细胞凋亡并降低了细胞存活率。我们还显示，DDX43通过去甲基化调节H19的表达，沉默H19抑制细胞存活。综上，这些结果表明，DDX43通过增强细胞存活，集落形成和抑制细胞凋亡为CML的发展提供了关键的支持，从而暗示DDX43作为CML的潜在治疗靶标。