Li Yang, Huang Hanying, Zhu Ziang, Chen Shuzhao, Liang Yang, Shu Lingling
State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, P.R. China.
Department of Hematological Oncology, Sun Yat-sen University Cancer Center, Guangzhou 510060, P.R. China.
iScience. 2023 Jul 22;26(8):107451. doi: 10.1016/j.isci.2023.107451. eCollection 2023 Aug 18.
Acute myeloid leukemia (AML) is the type of hematologic neoplasm most common in adults. Glucocorticoid-induced gene regulates cell proliferation through its function as a transcription factor. However, there is no consensus on the prognostic and immunoregulatory significance of in AML. In the present study, we evaluated the correlation between expression, immunoinfiltration, and prognostic significance in AML. Knockdown of significantly attenuated the proliferation of Hel cells and increased sensitivity to cytarabine (Ara-c) drugs. Furthermore, reduced the release of interleukin-1β (IL-1β) by inhibiting the NF-κB/NLRP3 signaling pathway, thereby inhibiting macrophage polarization to M1 subtype, and attenuating the pro-inflammatory tumor microenvironment. In conclusion, this study identified as an immune-related prognostic biomarker for AML patients and suggested that therapeutic targeting of may be a potential treatment option for AML through tumor immune escape.
急性髓系白血病（AML）是成人中最常见的血液肿瘤类型。糖皮质激素诱导基因作为转录因子通过其功能调节细胞增殖。然而，关于其在AML中的预后和免疫调节意义尚无共识。在本研究中，我们评估了其表达、免疫浸润与AML预后意义之间的相关性。敲低该基因显著减弱了Hel细胞的增殖并增加了对阿糖胞苷（Ara-c）药物的敏感性。此外，该基因通过抑制NF-κB/NLRP3信号通路减少白细胞介素-1β（IL-1β）的释放，从而抑制巨噬细胞向M1亚型极化，并减弱促炎性肿瘤微环境。总之，本研究确定该基因为AML患者的免疫相关预后生物标志物，并表明靶向该基因治疗可能是通过肿瘤免疫逃逸治疗AML的潜在选择。
