神经内分泌前列腺癌中谱系可塑性的分子机制研究进展

刘春钰, 邢毅飞. 神经内分泌前列腺癌中谱系可塑性的分子机制研究进展[J]. 临床泌尿外科杂志, 2023, 38(12): 973-978. doi: 10.13201/j.issn.1001-1420.2023.12.017
引用本文: 刘春钰, 邢毅飞. 神经内分泌前列腺癌中谱系可塑性的分子机制研究进展[J]. 临床泌尿外科杂志, 2023, 38(12): 973-978. doi: 10.13201/j.issn.1001-1420.2023.12.017
LIU Chunyu, XING Yifei. Research progress on molecular mechanism of lineage plasticity in neuroendocrine prostate cancer[J]. J Clin Urol, 2023, 38(12): 973-978. doi: 10.13201/j.issn.1001-1420.2023.12.017
Citation: LIU Chunyu, XING Yifei. Research progress on molecular mechanism of lineage plasticity in neuroendocrine prostate cancer[J]. J Clin Urol, 2023, 38(12): 973-978. doi: 10.13201/j.issn.1001-1420.2023.12.017

神经内分泌前列腺癌中谱系可塑性的分子机制研究进展

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Research progress on molecular mechanism of lineage plasticity in neuroendocrine prostate cancer

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  • 前列腺癌是一种激素驱动的疾病,其发生发展高度依赖于雄激素受体信号通路的活化,因而雄激素剥夺疗法成为晚期前列腺癌的治疗基石。雄激素剥夺疗法在治疗初期一般疗效良好,但随着治疗时间延长,部分患者进展为侵袭性极强的神经内分泌性前列腺癌,其诊断后的中位生存期不足1年。神经内分泌前列腺癌通常表现出雄激素受体的缺失、细胞干性增加以及神经内分泌标记物如嗜铬粒蛋白A、突触素和CD56的表达增加。神经内分泌前列腺癌目前尚未有特定的的治疗策略,主要应用具有相似神经内分泌表型的小细胞肺癌的铂类治疗方案,然而,铂类治疗并未在神经内分泌前列腺癌上取得满意的效果。本综述回顾了在神经内分泌前列腺癌中谱系可塑性发生的分子机制,包括基因突变、转录网络调控、表观遗传修饰改变等,为其潜在治疗策略提供见解。
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  • [1]

    Sung H, Ferlay J, Siegel RL, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J]. CA Cancer J Clin, 2021, 71(3): 209-249. doi: 10.3322/caac.21660

    [2]

    Sandhu S, Moore CM, Chiong E, et al. Prostate cancer[J]. Lancet, 2021, 398(10305): 1075-1090. doi: 10.1016/S0140-6736(21)00950-8

    [3]

    Pienta KJ, Bradley D. Mechanisms underlying the development of androgen-independent prostate cancer[J]. Clin Cancer Res, 2006, 12(6): 1665-1671. doi: 10.1158/1078-0432.CCR-06-0067

    [4]

    Davies A, Conteduca V, Zoubeidi A, et al. Biological evolution of castration-resistant prostate cancer[J]. Eur Urol Focus, 2019, 5(2): 147-154. doi: 10.1016/j.euf.2019.01.016

    [5]

    Wang Y, Wang Y, Ci XP, et al. Molecular events in neuroendocrine prostate cancer development[J]. Nat Rev Urol, 2021, 18(10): 581-596. doi: 10.1038/s41585-021-00490-0

    [6]

    Penson DF, Armstrong AJ, Concepcion R, et al. Enzalutamide versus bicalutamide in castration-resistant prostate cancer: the STRIVE trial[J]. J Clin Oncol, 2016, 34(18): 2098-2106. doi: 10.1200/JCO.2015.64.9285

    [7]

    Davies AH, Beltran H, Zoubeidi A. Cellular plasticity and the neuroendocrine phenotype in prostate cancer[J]. Nat Rev Urol, 2018, 15(5): 271-286. doi: 10.1038/nrurol.2018.22

    [8]

    Beltran H, Rickman D, Park K, et al. Molecular characterization of neuroendocrine prostate cancer(NEPC)and identification of new drug targets[J]. J Clin Oncol, 2011, 29(15_suppl): 4536. doi: 10.1200/jco.2011.29.15_suppl.4536

    [9]

    Storck WK, May AM, Westbrook TC, et al. The role of epigenetic change in therapy-induced neuroendocrine prostate cancer lineage plasticity[J]. Front Endocrinol, 2022, 13: 926585. doi: 10.3389/fendo.2022.926585

    [10]

    Cheng Q, Butler W, Zhou Y, et al. Pre-existing Castration-resistant Prostate Cancer-like Cells in Primary Prostate Cancer Promote Resistance to Hormonal Therapy[J]. Eur Urol, 2022, 81(5): 446-455. doi: 10.1016/j.eururo.2021.12.039

    [11]

    Abalde-Cela S, Piairo P, Diéguez L. The significance of circulating tumour cells in the clinic[J]. Acta Cytol, 2019, 63(6): 466-478. doi: 10.1159/000495417

    [12]

    Gazdar AF, Bunn PA, Minna JD. Small-cell lung cancer: what we know, what we need to know and the path forward[J]. Nat Rev Cancer, 2017, 17(12): 725-737. doi: 10.1038/nrc.2017.87

    [13]

    Qian JQ, Hirasawa K, Bostwick DG, et al. Loss of p53 and c-myc overrepresentation in stage T(2-3) N(1-3) M(0) prostate cancer are potential markers for cancer progression[J]. Mod Pathol, 2002, 15(1): 35-44. doi: 10.1038/modpathol.3880487

    [14]

    Ku SY, Rosario S, Wang Y, et al. Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance[J]. Science, 2017, 355(6320): 78-83. doi: 10.1126/science.aah4199

    [15]

    Zhou ZX, Flesken-Nikitin A, Corney DC, et al. Synergy of p53 and Rb deficiency in a conditional mouse model for metastatic prostate cancer[J]. Cancer Res, 2006, 66(16): 7889-7898. doi: 10.1158/0008-5472.CAN-06-0486

    [16]

    Zou M, Toivanen R, Mitrofanova A, et al. Transdifferentiation as a mechanism of treatment resistance in a mouse model of castration-resistant prostate cancer[J]. Cancer Discov, 2017, 7(7): 736-749. doi: 10.1158/2159-8290.CD-16-1174

    [17]

    Mosquera JM, Beltran H, Park K, et al. Concurrent AURKA and MYCN gene amplifications are harbingers of lethal TreatmentRelated neuroendocrine prostate cancer[J]. Neoplasia, 2013, 15(1): 1-IN4. doi: 10.1593/neo.121550

    [18]

    Lee JK, Phillips JW, Smith BA, et al. N-myc drives neuroendocrine prostate cancer initiated from human prostate epithelial cells[J]. Cancer Cell, 2016, 29(4): 536-547. doi: 10.1016/j.ccell.2016.03.001

    [19]

    Dardenne E, Beltran H, Benelli M, et al. N-myc induces an EZH2-mediated transcriptional program driving neuroendocrine prostate cancer[J]. Cancer Cell, 2016, 30(4): 563-577. doi: 10.1016/j.ccell.2016.09.005

    [20]

    Beltran H, Oromendia C, Danila DC, et al. A phase Ⅱ trial of the aurora kinase A inhibitor alisertib for patients with castration-resistant and neuroendocrine prostate cancer: efficacy and biomarkers[J]. Clin Cancer Res, 2019, 25(1): 43-51. doi: 10.1158/1078-0432.CCR-18-1912

    [21]

    Ton AT, Foo J, Singh K, et al. Development of VPC-70619, a small-molecule N-myc inhibitor as a potential therapy for neuroendocrine prostate cancer[J]. Int J Mol Sci, 2022, 23(5): 2588. doi: 10.3390/ijms23052588

    [22]

    Park JW, Lee JK, Witte ON, et al. FOXA2 is a sensitive and specific marker for small cell neuroendocrine carcinoma of the prostate[J]. Mod Pathol, 2017, 30(9): 1262-1272. doi: 10.1038/modpathol.2017.44

    [23]

    Qi JF, Nakayama K, Cardiff RD, et al. Siah2-dependent concerted activity of HIF and FoxA2 regulates formation of neuroendocrine phenotype and neuroendocrine prostate tumors[J]. Cancer Cell, 2010, 18(1): 23-38. doi: 10.1016/j.ccr.2010.05.024

    [24]

    Liu QL, Pang JA, Wang LA, et al. Histone demethylase PHF8 drives neuroendocrine prostate cancer progression by epigenetically upregulating FOXA2[J]. J Pathol, 2021, 253(1): 106-118. doi: 10.1002/path.5557

    [25]

    Grimm D, Bauer J, Wise P, et al. The role of SOX family members in solid tumours and metastasis[J]. Semin Cancer Biol, 2020, 67(Pt 1): 122-153.

    [26]

    Metz EP, Wilder PJ, Dong JX, et al. Elevating SOX2 in prostate tumor cells upregulates expression of neuroendocrine genes, but does not reduce the inhibitory effects of enzalutamide[J]. J Cell Physiol, 2020, 235(4): 3731-3740. doi: 10.1002/jcp.29267

    [27]

    Kregel S, Kiriluk KJ, Rosen AM, et al. Sox2 is an androgen receptor-repressed gene that promotes castration-resistant prostate cancer[J]. PLoS One, 2013, 8(1): e53701. doi: 10.1371/journal.pone.0053701

    [28]

    Bishop JL, Thaper D, Vahid S, et al. The master neural transcription factor BRN2is an androgen receptor-suppressed driver of neuroendocrine differentiation in prostate cancer[J]. Cancer Discov, 2017, 7(1): 54-71. doi: 10.1158/2159-8290.CD-15-1263

    [29]

    Bhagirath D, Yang TL, Tabatabai ZL, et al. BRN4 is a novel driver of neuroendocrine differentiation in castration-resistant prostate cancer and is selectively released in extracellular vesicles with BRN2[J]. Clin Cancer Res, 2019, 25(21): 6532-6545. doi: 10.1158/1078-0432.CCR-19-0498

    [30]

    Guo HY, Ci XP, Ahmed M, et al. ONECUT2 is a driver of neuroendocrine prostate cancer[J]. Nat Commun, 2019, 10: 278. doi: 10.1038/s41467-018-08133-6

    [31]

    Rotinen M, You S, Yang JL, et al. ONECUT2 is a targetable master regulator of lethal prostate cancer that suppresses the androgen axis[J]. Nat Med, 2018, 24(12): 1887-1898. doi: 10.1038/s41591-018-0241-1

    [32]

    Balanis NG, Sheu KM, Esedebe FN, et al. Pan-cancer convergence to a small-cell neuroendocrine phenotype that shares susceptibilities with hematological malignancies[J]. Cancer Cell, 2019, 36(1): 17-34.e7. doi: 10.1016/j.ccell.2019.06.005

    [33]

    Baca SC, Takeda DY, Seo JH, et al. Reprogramming of the FOXA1 cistrome in treatment-emergent neuroendocrine prostate cancer[J]. Nat Commun, 2021, 12(1): 1979. doi: 10.1038/s41467-021-22139-7

    [34]

    Brady NJ, Bagadion AM, Singh R, et al. Temporal evolution of cellular heterogeneity during the progression to advanced AR-negative prostate cancer[J]. Nat Commun, 2021, 12: 3372. doi: 10.1038/s41467-021-23780-y

    [35]

    Cejas P, Xie YT, Font-Tello A, et al. Subtype heterogeneity and epigenetic convergence in neuroendocrine prostate cancer[J]. Nat Commun, 2021, 12(1): 5775. doi: 10.1038/s41467-021-26042-z

    [36]

    Yegnasubramanian S, Haffner MC, Zhang YG, et al. DNA hypomethylation arises later in prostate cancer progression than CpG island hypermethylation and contributes to metastatic tumor heterogeneity[J]. Cancer Res, 2008, 68(21): 8954-8967. doi: 10.1158/0008-5472.CAN-07-6088

    [37]

    Ebihara T, Song C, Ryu SH, et al. Runx3 specifies lineage commitment of innate lymphoid cells[J]. Nat Immunol, 2015, 16(11): 1124-1133. doi: 10.1038/ni.3272

    [38]

    Mahapatra S, Klee EW, Young CY, et al. Global methylation profiling for risk prediction of prostate cancer[J]. Clin Cancer Res, 2012, 18(10): 2882-2895. doi: 10.1158/1078-0432.CCR-11-2090

    [39]

    Beltran H, Romanel A, Conteduca V, et al. Circulating tumor DNA profile recognizes transformation to castration-resistant neuroendocrine prostate cancer[J]. J Clin Investig, 2020, 130(4): 1653-1668. doi: 10.1172/JCI131041

    [40]

    McCabe MT, Davis JN, Day ML. Regulation of DNA methyltransferase 1 by the pRb/E2F1 pathway[J]. Cancer Res, 2005, 65(9): 3624-3632. doi: 10.1158/0008-5472.CAN-04-2158

    [41]

    Kinoshita H, Shi Y, Sandefur C, et al. Methylation of the androgen receptor minimal promoter silences transcription in human prostate cancer[J]. Cancer Res, 2000, 60(13): 3623-3630.

    [42]

    Kim DH, Sun D, Storck WK, et al. BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program[J]. Clin Cancer Res, 2021, 27(17): 4923-4936. doi: 10.1158/1078-0432.CCR-20-4968

    [43]

    Kleb B, Estécio MRH, Zhang JX, et al. Differentially methylated genes and androgen receptor re-expression in small cell prostate carcinomas[J]. Epigenetics, 2016, 11(3): 184-193. doi: 10.1080/15592294.2016.1146851

    [44]

    Clermont PL, Lin D, Crea F, et al. Polycomb-mediated silencing in neuroendocrine prostate cancer[J]. Clin Epigenetics, 2015, 7(1): 40. doi: 10.1186/s13148-015-0074-4

    [45]

    Ballas N, Grunseich C, Lu DD, et al. REST and its corepressors mediate plasticity of neuronal gene chromatin throughout neurogenesis[J]. Cell, 2005, 121(4): 645-657. doi: 10.1016/j.cell.2005.03.013

    [46]

    Zhang X, Coleman IM, Brown LG, et al. SRRM4 Expression and the Loss of REST Activity May Promote the Emergence of the Neuroendocrine Phenotype in Castration-Resistant Prostate Cancer[J]. Clin Cancer Res, 2015, 21(20): 4698-4708. doi: 10.1158/1078-0432.CCR-15-0157

    [47]

    Raj B, Irimia M, Braunschweig U, et al. A global regulatory mechanism for activating an exon network required for neurogenesis[J]. Mol Cell, 2014, 56(1): 90-103. doi: 10.1016/j.molcel.2014.08.011

    [48]

    Lee AR, Gan Y, Tang YX, et al. A novel mechanism of SRRM4 in promoting neuroendocrine prostate cancer development via a pluripotency gene network[J]. EBioMedicine, 2018, 35: 167-177. doi: 10.1016/j.ebiom.2018.08.011

    [49]

    Hsu EC, Rice MA, Bermudez A, et al. Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1[J]. Proc Natl Acad Sci U S A, 2020, 117(4): 2032-2042. doi: 10.1073/pnas.1905384117

    [50]

    Lee CF, Chen Y, Hernandez E, et al. The central role of Sphingosine kinase 1 in the development of neuroendocrine prostate cancer(NEPC): a new targeted therapy of NEPC[J]. Clin Transl Med, 2022, 12(2): e695. doi: 10.1002/ctm2.695

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出版历程
收稿日期:  2023-10-05
刊出日期:  2023-12-06

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