Abstract A12: Androgen receptor inhibition is involved in Finasteride-reduced AML cell proliferation

IF 11.5 Q1 HEMATOLOGY
Pang-Ting Cheng, C. Teng, Y. Cheng, Mei-Chih Chen, Ho Lin
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引用次数: 0

Abstract

Acute myeloid leukemia (AML) is a top priority type of hematological malignancies to be studied and treated. Androgen receptor (AR) plays important roles in various cancers, such as types of the prostate, breast, liver, and lung. However, the role of AR in leukemia is so far uncertain. Finasteride is a 5 alpha-reductase inhibitor for reduction of cellular 5 alpha-dihydrotestosterone production and commonly used to treat benign prostatic hyperplasia for decades. Here, the data showed that Finasteride treatment significantly decreased the proliferation of AML cell lines, including KG-1 and HL-60. More specific to its impact on androgen’s actions, the authors found that Finasteride inhibited the phosphorylation and activation of AR, while the cell cycle-related proteins such as CDK1, Cyclin A, and p21 were unaffected. Interestingly, the increase of AKT phosphorylation was observed after Finasteride treatment, which is correspondent to the previous findings of mutual correlations between AR inhibition and AKT activation in prostate cancer cells. It implies that AR might play a physiological role in AML cells for proliferation, in which AR closely collaborates with AKT for a balance of regulation. In summary, these results suggest that Finasteride might reduce the proliferation of AML cell lines through AR inhibition. These findings could be helpful to uncover novel AML treatments in the future. Citation Format: Pang-Ting Cheng, Chieh-Lin Jerry Teng, Yu-Chiao Cheng, Mei-Chih Chen, Ho Lin. Androgen receptor inhibition is involved in Finasteride-reduced AML cell proliferation [abstract]. In: Proceedings of the AACR Special Conference: Acute Myeloid Leukemia and Myelodysplastic Syndrome; 2023 Jan 23-25; Austin, TX. Philadelphia (PA): AACR; Blood Cancer Discov 2023;4(3_Suppl):Abstract nr A12.
摘要A12:雄激素受体抑制与非那雄胺降低AML细胞增殖有关
急性髓细胞白血病(AML)是需要研究和治疗的血液系统恶性肿瘤的首要类型。雄激素受体(AR)在各种癌症中起着重要作用,如前列腺癌、乳腺癌、肝癌和肺癌。然而,到目前为止,AR在白血病中的作用还不确定。非那雄胺是一种5α还原酶抑制剂,可减少细胞5α二氢睾酮的产生,几十年来常用于治疗良性前列腺增生。数据显示,非那雄胺处理显著降低了AML细胞系的增殖,包括KG-1和HL-60。更具体地说,作者发现非那雄胺抑制AR的磷酸化和活化,而细胞周期相关蛋白如CDK1、细胞周期蛋白A和p21不受影响。有趣的是,在非那雄胺治疗后观察到AKT磷酸化的增加,这与之前在前列腺癌症细胞中AR抑制和AKT激活之间相互关联的发现一致。这意味着AR可能在AML细胞增殖中发挥生理作用,其中AR与AKT密切合作以实现调节平衡。总之,这些结果表明,非那雄胺可能通过抑制AR来减少AML细胞系的增殖。这些发现可能有助于揭示未来新的AML治疗方法。引文格式:彭廷成,陈,何林。非那雄胺抑制AML细胞增殖与雄激素受体抑制有关[摘要]。载:AACR特别会议论文集:急性髓细胞白血病和骨髓增生异常综合征;2023年1月23日至25日;德克萨斯州奥斯汀。费城(PA):AACR;血液癌症Discov 2023;4(3_Suppl):摘要编号A12。
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来源期刊
CiteScore
12.70
自引率
1.80%
发文量
139
期刊介绍: The journal Blood Cancer Discovery publishes high-quality Research Articles and Briefs that focus on major advances in basic, translational, and clinical research of leukemia, lymphoma, myeloma, and associated diseases. The topics covered include molecular and cellular features of pathogenesis, therapy response and relapse, transcriptional circuits, stem cells, differentiation, microenvironment, metabolism, immunity, mutagenesis, and clonal evolution. These subjects are investigated in both animal disease models and high-dimensional clinical data landscapes. The journal also welcomes submissions on new pharmacological, biological, and living cell therapies, as well as new diagnostic tools. They are interested in prognostic, diagnostic, and pharmacodynamic biomarkers, and computational and machine learning approaches to personalized medicine. The scope of submissions ranges from preclinical proof of concept to clinical trials and real-world evidence. Blood Cancer Discovery serves as a forum for diverse ideas that shape future research directions in hematooncology. In addition to Research Articles and Briefs, the journal also publishes Reviews, Perspectives, and Commentaries on topics of broad interest in the field.
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