Yan Zijun, Xia Jie, Cao Ziyang, Zhang Hongyang, Wang Jinxia, Feng Tienan, Shu Yi, Zou Lin
Clinical Research Unit, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200062, China.
Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai 200062, China.
Genes Dis. 2023 Apr 26;11(5):100949. doi: 10.1016/j.gendis.2023.03.022. eCollection 2024 Sep.
T-cell acute lymphoblastic leukemia (T-ALL), a heterogeneous hematological malignancy, is caused by the developmental arrest of normal T-cell progenitors. The development of targeted therapeutic regimens is impeded by poor knowledge of the stage-specific aberrances in this disease. In this study, we performed multi-omics integration analysis, which included mRNA expression, chromatin accessibility, and gene-dependency database analyses, to identify potential stage-specific druggable targets and repositioned drugs for this disease. This multi-omics integration helped identify 29 potential pathological genes for T-ALL. These genes exhibited tissue-specific expression profiles and were enriched in the cell cycle, hematopoietic stem cell differentiation, and the AMPK signaling pathway. Of these, four known druggable targets (CDK6, TUBA1A, TUBB, and TYMS) showed dysregulated and stage-specific expression in malignant T cells and may serve as stage-specific targets in T-ALL. The TUBA1A expression level was higher in the early T cell precursor (ETP)-ALL cells, while TUBB and TYMS were mainly highly expressed in malignant T cells arrested at the CD4 and CD8 double-positive or single-positive stage. CDK6 exhibited a U-shaped expression pattern in malignant T cells along the naïve to maturation stages. Furthermore, mebendazole and gemcitabine, which target TUBA1A and TYMS, respectively, exerted stage-specific inhibitory effects on T-ALL cell lines, indicating their potential stage-specific antileukemic role in T-ALL. Collectively, our findings might aid in identifying potential stage-specific druggable targets and are promising for achieving more precise therapeutic strategies for T-ALL.
T细胞急性淋巴细胞白血病(T-ALL)是一种异质性血液系统恶性肿瘤,由正常T细胞祖细胞的发育停滞引起。由于对该疾病阶段特异性异常的了解不足,阻碍了靶向治疗方案的发展。在本研究中,我们进行了多组学整合分析,包括mRNA表达、染色质可及性和基因依赖性数据库分析,以确定该疾病潜在的阶段特异性可药物化靶点和重新定位的药物。这种多组学整合有助于识别29个T-ALL潜在病理基因。这些基因表现出组织特异性表达谱,并在细胞周期、造血干细胞分化和AMPK信号通路中富集。其中,四个已知的可药物化靶点(CDK6、TUBA1A、TUBB和TYMS)在恶性T细胞中显示出失调的阶段特异性表达,可能作为T-ALL的阶段特异性靶点。TUBA1A在早期T细胞前体(ETP)-ALL细胞中的表达水平较高,而TUBB和TYMS主要在停滞于CD4和CD8双阳性或单阳性阶段的恶性T细胞中高表达。CDK6在恶性T细胞从幼稚到成熟阶段呈现U形表达模式。此外,分别靶向TUBA1A和TYMS的甲苯咪唑和吉西他滨对T-ALL细胞系发挥了阶段特异性抑制作用,表明它们在T-ALL中具有潜在的阶段特异性抗白血病作用。总的来说,我们的发现可能有助于识别潜在的阶段特异性可药物化靶点,并有望为T-ALL实现更精确的治疗策略。