Pang-Ting Cheng, C. Teng, Y. Cheng, Mei-Chih Chen, Ho Lin
{"title":"摘要A12:雄激素受体抑制与非那雄胺降低AML细胞增殖有关","authors":"Pang-Ting Cheng, C. Teng, Y. Cheng, Mei-Chih Chen, Ho Lin","doi":"10.1158/2643-3249.aml23-a12","DOIUrl":null,"url":null,"abstract":"\n 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.\n 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.","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":11.5000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Abstract A12: Androgen receptor inhibition is involved in Finasteride-reduced AML cell proliferation\",\"authors\":\"Pang-Ting Cheng, C. Teng, Y. Cheng, Mei-Chih Chen, Ho Lin\",\"doi\":\"10.1158/2643-3249.aml23-a12\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"\\n 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.\\n 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. 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Abstract A12: Androgen receptor inhibition is involved in Finasteride-reduced AML cell proliferation
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.
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.