留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

Retinoid X receptor signaling pathway in leukemia

Lu Xiaoxi Ma Zhigui Gao Ju Zhu Yiping

陆晓茜, 马志贵, 高举, 等. 维A酸X受体信号通路与白血病[J]. 器官移植, 2014, 5(6): 383-388. doi: 10.3969/j.issn.1674-7445.2014.06.013
引用本文: 陆晓茜, 马志贵, 高举, 等. 维A酸X受体信号通路与白血病[J]. 器官移植, 2014, 5(6): 383-388. doi: 10.3969/j.issn.1674-7445.2014.06.013
Lu Xiaoxi, Ma Zhigui, Gao Ju, et al. Retinoid X receptor signaling pathway in leukemia[J]. ORGAN TRANSPLANTATION, 2014, 5(6): 383-388. doi: 10.3969/j.issn.1674-7445.2014.06.013
Citation: Lu Xiaoxi, Ma Zhigui, Gao Ju, et al. Retinoid X receptor signaling pathway in leukemia[J]. ORGAN TRANSPLANTATION, 2014, 5(6): 383-388. doi: 10.3969/j.issn.1674-7445.2014.06.013

维A酸X受体信号通路与白血病

doi: 10.3969/j.issn.1674-7445.2014.06.013
基金项目: 

National Natural Science Foundation 81000215

The technology bureau of Chengdu 11DXYB086JH-027

详细信息
    通讯作者:

    朱易萍, Email:yipingzhu918@qq.com

  • 中图分类号: R617

Retinoid X receptor signaling pathway in leukemia

Funds: 

National Natural Science Foundation 81000215

The technology bureau of Chengdu 11DXYB086JH-027

More Information
  • 摘要: 维A酸X受体(RXR)是配体依赖的核转录因子, 在调节一系列生理病理过程中起重要作用。在分子水平上, RXR与多个信号通路相互作用, 调控细胞生长、分化、生存与死亡等靶基因的表达。RXR信号通路网络与其他信号通路之间的相互作用使RXR成为抗肿瘤药物作用的新靶点。本文就RXR信号通路在白血病发生发展中的作用进行简要综述。

     

  • Figure  1.  Simplified diagram of the RXR/RAR signaling network

    Cyclic adenosine monophosphate(cAMP)-protein kinase A (PKA) signal pathway activation induce leukemia cell apoptosis and differentiation. Janus kinase-signal transducer and activator of transcription (JAK-STAT) 3 signal pathway induce leukemia cells apoptosis. Activate MEK pathway show different effect on gene transcription mediated by RXRE

  • [1] Evans RM, Mangelsdorf DJ. Nuclear receptors, RXR, and the big bang[J]. Cell, 2014, 157(1):255-266. doi: 10.1016/j.cell.2014.03.012
    [2] Piskunov A, Al Tanoury Z, Rochette-Egly C. Nuclear and extra-nuclear effects of retinoid acid receptors: how they are interconnected[J]. Subcell Biochem, 2014, 70:103-127. doi: 10.1007/978-94-017-9050-5
    [3] le Maire A, Bourguet W. Retinoic acid receptors: structural basis for coregulator interaction and exchange[J]. Subcell Biochem, 2014, 70:37-54. doi: 10.1007/978-94-017-9050-5
    [4] Rastinejad F. Retinoid X receptor and its partners in the nuclear receptor family[J]. Curr Opin Struct Biol, 2001, 11(1):33-38. doi: 10.1016/S0959-440X(00)00165-2
    [5] Thomas M, Sukhai MA, Kamel-Reid S. An emerging role for retinoid X receptor α in malignant hematopoiesis[J]. Leuk Res, 2012, 36(9):1075-1081. doi: 10.1016/j.leukres.2012.05.022
    [6] Altucci L, Leibowitz MD, Ogilvie KM, et al. RAR and RXR modulation in cancer and metabolic disease[J]. Nat Rev Drug Discov, 2007, 6(10):793-810. doi: 10.1038/nrd2397
    [7] Tedesco J, Qualtieri J, Head D, et al. High prevalence of obesity in acute promyelocytic leukemia (APL): implications for differentiating agents in APL and metabolic syndrome[J]. Ther Adv Hematol, 2011, 2(3):141-145. doi: 10.1177/2040620711408490
    [8] Wang ZY, Chen Z. Acute promyelocytic leukemia: from highly fatal to highly curable[J]. Blood, 2008, 111(5):2505-2515. doi: 10.1182/blood-2007-07-102798
    [9] Zeisig BB, Kwok C, Zelent A, et al. Recruitment of RXR by homotetrameric RARalpha fusion proteins is essential for transformation[J]. Cancer Cell, 2007, 12(1):36-51. doi: 10.1016/j.ccr.2007.06.006
    [10] Dong S, Stenoien DL, Qiu J, et al. Reduced intranuclear mobility of APL fusion proteins accompanies their mislocalization and results in sequestration and decreased mobility of retinoid X receptor alpha[J]. Mol Cell Biol, 2004, 24(10):4465-4475. doi: 10.1128/MCB.24.10.4465-4475.2004
    [11] Qiu JJ, Lu X, Zeisig BB, et al. Leukemic transformation by the APL fusion protein PRKAR1A-RAR{alpha} critically depends on recruitment of RXR{alpha}[J].Blood, 2010, 115(3):643-652. doi: 10.1182/blood-2009-07-232652
    [12] Rush EA, Pollock SL, Abecassis I, et al. Interaction with RXR is necessary for NPM-RAR-induced myeloid differentiation blockade[J]. Leuk Res, 2013, 37(12):1704-1710. doi: 10.1016/j.leukres.2013.09.024
    [13] Glass CK, Rosenfeld MG. The coregulator exchange in transcriptional functions of nuclear receptors[J]. Genes Dev, 2000, 14(2):121-141. http://cn.bing.com/academic/profile?id=2156575042&encoded=0&v=paper_preview&mkt=zh-cn
    [14] Perissi V, Rosenfeld MG. Controlling nuclear receptors: the circular logic of cofactor cycles[J]. Nat Rev Mol Cell Biol, 2005, 6(7):542-554. doi: 10.1038/nrm1680
    [15] Laursen KB, Wong PM, Gudas LJ. Epigenetic regulation by RARα maintains ligand-independent transcriptional activity[J]. Nucleic Acids Res, 2012, 40(1):102-115. doi: 10.1093/nar/gkr637
    [16] Lengfelder E, Saussele S, Weisser A, et al. Treatment concepts of acute promyelocytic leukemia[J]. Crit Rev Oncol Hematol, 2005, 56(2):261-274. doi: 10.1016/j.critrevonc.2004.08.009
    [17] Altucci L, Rossin A, Raffelsberger W, et al. Retinoic acid-induced apoptosis in leukemia cells is mediated by paracrine action of tumor-selective death ligand TRAIL[J]. Nat Med, 2001, 7(6):680-686. doi: 10.1038/89050
    [18] Altucci L, Gronemeyer H. Retinoids and TRAIL: two cooperating actors to fight against cancer[J]. Vitam Horm, 2004, 67:319-345. doi: 10.1016/S0083-6729(04)67017-8
    [19] Zhu J, Nasr R, Pérès L, et al. RXR is an essential component of the oncogenic PML/RARA complex in vivo[J]. Cancer Cell, 2007, 12(1):23-35. doi: 10.1016/j.ccr.2007.06.004
    [20] Tanaka T, De Luca LM. Therapeutic potential of "rexinoids" in cancer prevention and treatment[J]. Cancer Res, 2009, 69(12):4945-4947. doi: 10.1158/0008-5472.CAN-08-4407
    [21] Rice KL, de Thé H. The acute promyelocytic leukaemia success story: curing leukaemia through targeted therapies[J]. J Intern Med, 2014, 276(1):61-70. doi: 10.1111/joim.12208
    [22] Guillemin MC, Raffoux E, Vitoux D, et al. Invo activation of cAMP signaling induces growth arrest and differentiation in acute promyelocytic leukemia[J]. J Exp Med, 2002, 196(10):1373-1380. doi: 10.1084/jem.20021129
    [23] Zhao Q, Tao J, Zhu Q, et al. Rapid induction of cAMP/PKA pathway during retinoic acid-induced acute promyelocytic leukemia cell differentiation[J]. Leukemia, 2004, 18(2):285-292. doi: 10.1038/sj.leu.2403226
    [24] Altucci L, Rossin A, Hirsch O, et al. Rexinoid-triggered differentiation and tumor-selective apoptosis of acute myeloid leukemia by protein kinase A-mediated desubordination of retinoid X receptor[J]. Cancer Res, 2005, 65(19):8754-8765. doi: 10.1158/0008-5472.CAN-04-3569
    [25] Kamashev D, Vitoux D, De Thé H. PML-RARA-RXR oligomers mediate retinoid and rexinoid/cAMP cross-talk in acute promyelocytic leukemia cell differentiation[J]. J Exp Med, 2004, 199(8):1163-1174. doi: 10.1084/jem.20032226
    [26] Gaillard E, Bruck N, Brelivet Y, et al. Phosphorylation by PKA potentiates retinoic acid receptor alpha activity by means of increasing interaction with and phosphorylation by cyclin H/cdk7[J]. Proc Natl Acad Sci U S A, 2006, 103(25):9548-9553. doi: 10.1073/pnas.0509717103
    [27] Nasr R, Guillemin MC, Ferhi O, et al. Eradication of acute promyelocytic leukemia-initiating cells through PML-RARA degradation[J]. Nat Med, 2008, 14(12):1333-1342. doi: 10.1038/nm.1891
    [28] Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosin[J]. Lancet, 2005, 365(9464):1054-1061. doi: 10.1016/S0140-6736(05)74230-6
    [29] Campbell PJ, Baxter EJ, Beer PA, et al. Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformation[J]. Blood, 2006, 108(10):3548-3555. doi: 10.1182/blood-2005-12-013748
    [30] Gaikwad A, Rye CL, Devidas M, et al. Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia[J]. Br J Haematol, 2009, 144(6):930-932. doi: 10.1111/bjh.2009.144.issue-6
    [31] Hornakova T, Staerk J, Royer Y, et al. Acute lymphoblastic leukemia-associated JAK1 mutants activate the Janus kinase/STAT pathway via interleukin-9 receptor alpha homodimers[J]. J Biol Chem, 2009, 284(11):6773-6781. doi: 10.1074/jbc.M807531200
    [32] Hughes PJ, Zhao Y, Chandraratna RA, et al. Retinoid-mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARalpha and RXR and involves the phosphoinositide 3-kinase and ERK-MAP kinase pathways[J]. J Cell Biochem, 2006, 97(2):327-350. doi: 10.1002/(ISSN)1097-4644
    [33] Mann KK, Padovani AM, Guo Q, et al. Arsenic trioxide inhibits nuclear receptor function via SEK1/JNK-mediated RXRalpha phosphorylation[J]. J Clin Invest, 2005, 115(10):2924-2933. doi: 10.1172/JCI23628
    [34] Battle TE, Roberson MS, Zhang T, et al. Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation[J]. Eur J Cell Biol, 2001, 80(1):59-67. doi: 10.1078/0171-9335-00141
    [35] Park EJ, Kiselev E, Conda-Sheridan M, et al. Induction of apoptosis by 3-amino-6-(3-aminopropyl)-5, 6-dihydro-5, 11-dioxo-11H-indeno[1, 2-c]isoquinoline via modulation of MAPKs (p38 and c-Jun N-terminal kinase) and c-Myc in HL-60 human leukemia cells[J]. J Nat Prod, 2012, 75(3):378-384.
    [36] Rochette-Egly C. Nuclear receptors: integration of multiple signaling pathways through phosphorylation[J]. Cell Signal, 2003, 15(4):355-366. doi: 10.1016/S0898-6568(02)00115-8
    [37] Ishaq M, Fan M, Natarajan V. Accumulation of RXR alpha during activation of cycling human T lymphocytes: modulation of RXRE transactivation function by mitogen-activated protein kinase pathways[J]. J Immunol, 2000, 165(8):4217-4125. doi: 10.4049/jimmunol.165.8.4217
    [38] Ishaq M, Fan M, Wigmore K, et al. Regulation of retinoid X receptor responsive element-dependent transcription in T lymphocytes by Ser/Thr phosphatases: functional divergence of protein kinase C (PKC)theta; and PKC alpha in mediating calcineurin-induced transactivation[J]. J Immunol, 2002, 169(2):732-738. doi: 10.4049/jimmunol.169.2.732
  • 加载中
图(1)
计量
  • 文章访问数:  26
  • HTML全文浏览量:  24
  • PDF下载量:  4
  • 被引次数: 0
出版历程
  • 收稿日期:  2014-07-20
  • 网络出版日期:  2021-01-19
  • 刊出日期:  2014-11-15

目录

    /

    返回文章
    返回