Acute myeloid leukemia (AML) is a form of blood cancer that arise as a result of clonal proliferation of malignant myeloid precursors acquiring genetic abnormalities. Primary resistance to initial treatment and disease recurrence continues to be huge challenge in treating AML. Herein, GSE114868 was analyzed for differentially-expressed lncRNAs between AML patients’ mononucleated cells and healthy normal control mononucleated cells and 191 lncRNAs were significantly deregulated in AML patients’ mononucleated cells. The correlation between candidate lncRNAs and AML patients’ overall survival was analyzed and 6 lncRNAs, including MIR181A1HG, TRAF3IP2-AS1, STARD4-AS1, E2F3-IT1, FAM215A, and HHIP-AS1 were dramatically linked to AML patients’ OS. Using a Cox proportional-hazards model, we identified risk factors and found FAM215A as a risk factor for AML patients’ prognosis. The expression level of FAM215A showed to be upregulated within blood samples and cells. Genes correlated with FAM215A were correlated to cell division, modulation of cell apoptosis, and modulation of programmed cell death. FAM215A knockdown inhibited AML cell viability, elicited G0/G1-phase arrest of cell cycle, enhanced cell apoptosis, increased proapoptotic Bax and cleaved-caspase3 levels, and decreased antiapoptotic Bcl2. FAM215A overexpression exerted opposite effects on AML cells. Conclusively, FAM215A serves as an oncogenic lncRNA in AML, promoting cell viability, relieving cell cycle arrest, and suppressing cell apoptosis. FAM215A might be un underlying biological prognostic marker and therapeutic target for AML.

急性髓系白血病 (AML) 是一种血癌，是由于获得遗传异常的恶性髓系前体细胞的克隆增殖而引起的。对初始治疗的原发性耐药和疾病复发仍然是治疗 AML 的巨大挑战。在此，对 GSE114868 进行了 AML 患者单核细胞和健康正常对照单核细胞之间差异表达的 lncRNA 分析，191 个 lncRNA 在 AML 患者单核细胞中显着失调。分析了候选lncRNA与AML患者总生存率之间的相关性，包括MIR181A1HG、TRAF3IP2-AS1、STARD4-AS1、E2F3-IT1、FAM215A和HHIP-AS1在内的6种lncRNA与AML患者的OS显着相关。使用 Cox 比例风险模型，我们确定了风险因素，并发现 FAM215A 是 AML 患者预后的风险因素。FAM215A 的表达水平在血液样本和细胞中上调。与 FAM215A 相关的基因与细胞分裂、细胞凋亡的调节和程序性细胞死亡的调节相关。FAM215A 敲低可抑制 AML 细胞活力，引发细胞周期 G0/G1 期停滞，增强细胞凋亡，增加促凋亡 Bax 和 cleaved-caspase3 水平，并降低抗凋亡 Bcl2。FAM215A 过表达对 AML 细胞产生相反的作用。总之，FAM215A 在 AML 中充当致癌 lncRNA，促进细胞活力、缓解细胞周期停滞并抑制细胞凋亡。FAM215A 可能是 AML 潜在的生物预后标志物和治疗靶点。