Inhibition of brain metastasis by blocking MAPK12 driver kinase functions
Inhibition of brain metastasis by blocking MAPK12 driver kinase functions
批准号:
10172862
负责人:
Dihua Yu
金额:
$43.26万
依托单位国家:
美国
项目类别:
财政年份:
2017
资助国家:
美国
项目状态:
已结题
起止时间:
2017-06-01 至 2022-11-30
关键词:
AddressAffectAnimalsAreaBiological AssayBrainBreast Cancer CellBreast Cancer PatientBreast Cancer PreventionBreast Cancer TreatmentBreast Cancer cell lineBreast Cancer therapyBreast cancer metastasisCancer PatientCarotid ArteriesCellsChemicalsCitric Acid CycleClinicClinicalClinical TrialsDataDiagnosisDiseaseDisseminated Malignant NeoplasmEarly InterventionEnergy-Generating ResourcesFDA approvedFamilyFutureGenerationsGlucoseGoalsGrowthHumanImmunocompetentIncidenceLibrariesMAP Kinase GeneMAPK12 geneMDA MB 231Malignant NeoplasmsMediatingMetabolismMetastatic breast cancerMetastatic malignant neoplasm to brainMetastatic toMitochondriaModelingMusNeoplasm MetastasisNude MicePathway interactionsPatientsPharmacotherapyPhosphotransferasesPlayPopulationPreventionPrimary NeoplasmQuality of lifeRecurrenceRefractoryResearchRoleSignal PathwaySignal TransductionSystemic diseaseTestingTherapeutic AgentsTissuesTranslatingTrastuzumabWomananticancer researchbrain metabolismcancer cellcell motilityclinical applicationclinical careclinically relevantdrug developmenteffective therapyefficacy testingimprovedin vivoinhibitor/antagonistinsightkinase inhibitorloss of functionmalignant breast neoplasmmembermortalitynext generation sequencingnovelnovel therapeuticsoverexpressionpalliativetargeted treatmenttherapeutic targettumor progressionvector control
中文摘要
在每年160万名被诊断为乳腺癌的女性中,约有10%-16%发生脑转移。
即使有了最先进的临床护理,脑转移瘤患者一年的死亡率也高达20%。
生死存亡。目前,转移性难治性乳腺癌尚无有效的药物治疗。
大脑。因此,迫切需要新颖有效的治疗方法来治疗这一人群。不幸的是,
由于缺乏对脑转移瘤的深入了解,开发脑转移瘤的有效疗法在很大程度上受到了阻碍
脑转移的基本机制,可指导药物开发和临床试验。至
克服挑战,我们进行了史无前例的活体人类亲属组筛选,以揭示
促进小鼠乳腺癌脑转移的新的激酶,因为激酶位于中心结节
癌细胞信号网络对癌症进展/转移至关重要,并可作为治疗药物
目标。在我们确定的与侵袭性脑转移相关的首要候选激酶中,有丝分裂原-
活化蛋白激酶12(MAPK12,又称p38γ)在脑中的作用尚不清楚
但在高度侵袭性的人类乳腺癌和MAPK12高表达的患者中过表达。
表达乳腺癌的人以后脑转移的发生率更高。因此,我们表演了
使用MAPK12过表达的乳腺癌细胞进行实验性脑转移分析,并验证了
MAPK12确实促进了动物的脑转移。MAPK12是MAPK家族的成员,其
过度表达会增加癌细胞的运动性和侵袭性。令人兴奋的是,我们发现MAPK12位于
脑转移丰富的蛋白激酶信号网络的“中枢”,增强脑转移细胞
利用乳酸作为大脑生长的能量来源。此外,MAPK12具有靶向性
临床上用于治疗其他疾病的可用的抑制剂。这里,我们假设激活/
MAPK12的过表达协调乳腺癌细胞中的信号通路促进脑转移,
而MAPK12可通过临床应用的激酶抑制剂被有效地抑制。的主要目标
这一建议是:1)确定MAPK12在自发性脑转移瘤和免疫中的功能作用
称职的脑转移模型,并进一步验证其临床意义;2)研究新的
MAPK12活化机制探讨MAPK12介导乳腺癌脑转移的机制
脑转移癌细胞有效地利用乳酸作为适应和生长的能量来源
3)探索MAPK12作为治疗和/或预防乳腺癌的治疗靶点的潜力
癌症脑转移。这些研究的成功完成将带来对
乳腺癌脑转移和第一代有效的脑转移靶向治疗。
最终,我们的发现将顺利地转化为临床试验,导致新的更好的治疗方法
乳腺癌脑转移患者在绝望中寻找希望。
英文摘要
Among 1.6 million women diagnosed with breast cancer every year, about 10-16% develop brain metastasis.
Even with the most advanced clinical care, patients with brain metastasis have a devastating <20% one-year
survival. At present, no effective drug treatment exists for patients with refractory breast cancer metastatic to
the brain. Therefore, novel and effective therapies are urgently needed for this population. Unfortunately,
developing effective therapies for brain metastasis is largely hampered by a lack of in-depth understanding of
the basic mechanisms of brain metastasis, which could guide drug development and clinical trials. To
surmount the challenge, we have performed an unprecedented in vivo screen of the human kinome to uncover
novel kinases that promote breast cancer brain metastasis in mice, because kinases are at the central nodes
of cancer cell signaling networks critical for cancer progression/metastasis and are druggable as therapeutic
targets. Among the top candidate kinases associated with aggressive brain metastasis we identified, Mitogen-
Activated Protein Kinase 12 (MAPK12, also known as p38γ) was not previously known to play roles in brain
metastasis but is overexpressed in highly aggressive human breast cancers, and patients with MAPK12 high-
expressing breast cancers have higher incidences of brain metastasis later on. Therefore, we performed
experimental brain metastasis assays using MAPK12-overexpressing breast cancer cells, and validated that
MAPK12 indeed promotes brain metastasis in animals. MAPK12 is a member of the MAPK family and its
overexpression increases cancer cell motility and invasion. Excitingly, we identified that MAPK12 is located at
the "hub" of a signaling network of brain metastasis-enriched kinases that enhances brain metastatic cells’
utilization of lactate as an energy source for outgrowth in the brain. Furthermore, MAPK12 is targetable with
available inhibitors that are used in the clinic for other diseases. Here, we hypothesize that activation/
overexpression of MAPK12 coordinates signaling pathways in breast cancer cells to promote brain metastasis,
and MAPK12 may be effectively inhibited by using clinically applicable kinase inhibitors. The major goals of
this proposal are 1) Determine the functional roles of MAPK12 in spontaneous brain metastasis and in immune
competent brain metastasis models, and further validating their clinical relevance; 2) Investigate novel
mechanisms of MAPK12-mediated breast cancer brain metastasis by focusing on how MAPK12-activated
brain metastatic cancer cells efficiently use lactate as an energy source for adaptation and outgrowth in the
brain; 3) Explore the potential of MAPK12 as a therapeutic target for the treatment and/or prevention of breast
cancer brain metastasis. The successful completion of these studies will bring about new understanding of
breast cancer brain metastasis and the first generation of effective brain metastasis-targeted therapies.
Ultimately, our findings will be smoothly translated to clinical trials, leading to new and better treatments for
breast cancer brain metastasis patients in dire search of hope.
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DOI:
10.1016/j.pharmthera.2020.107753
发表时间:
2021-05
期刊:
Pharmacology & therapeutics
影响因子:
13.5
作者:
[Xiao Y, Yu D]
通讯作者:
Yu D
Targeting Aberrant p70S6K Activation for Estrogen Receptor-Negative Breast Cancer Prevention.
针对雌激素受体阴性乳腺癌预防的异常 p70S6K 激活。
DOI:
10.1158/1940-6207.capr-17-0106
发表时间:
2017
期刊:
Cancer prevention research (Philadelphia, Pa.)
影响因子:
--
作者:
[Wang,Xiao, Yao,Jun, Wang,Jinyang, Zhang,Qingling, Brady,SamuelW, Arun,Banu, Seewaldt,VictoriaL, Yu,Dihua]
通讯作者:
Yu,Dihua
DOI:
10.1158/0008-5472.can-17-2726
发表时间:
2018-05-01
期刊:
Cancer research
影响因子:
11.2
作者:
[Zhou Z, Li M, Zhang L, Zhao H, Şahin Ö, Chen J, Zhao JJ, Songyang Z, Yu D]
通讯作者:
Yu D
DOI:
10.1016/j.ccell.2021.11.002
发表时间:
2022-01-10
期刊:
Cancer cell
影响因子:
50.3
作者:
[Li H, Xiao Y, Li Q, Yao J, Yuan X, Zhang Y, Yin X, Saito Y, Fan H, Li P, Kuo WL, Halpin A, Gibbons DL, Yagita H, Zhao Z, Pang D, Ren G, Yee C, Lee JJ, Yu D]
通讯作者:
Yu D
DOI:
10.1126/scitranslmed.aaz5387
发表时间:
2020-05-27
期刊:
Science translational medicine
影响因子:
17.1
作者:
[Zhang L, Yao J, Wei Y, Zhou Z, Li P, Qu J, Badu-Nkansah A, Yuan X, Huang YW, Fukumura K, Mao X, Chang WC, Saunus J, Lakhani S, Huse JT, Hung MC, Yu D]
通讯作者:
Yu D
共 7 条
Exploring novel strategies for immunoprevention of estrogen receptor negative breast cancer
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批准号:10583390
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Combating Breast Cancer Brain Metastasis by Blocking the Two-Pronged Driver Kinase Function of CDK5
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Combating Breast Cancer Brain Metastasis by Blocking the Two-Pronged Driver Kinase Function of CDK5
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Inhibition of brain metastasis by blocking MAPK12 driver kinase functions
-
批准号:9308550
-
项目类别:
-
资助金额:$43.26万
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财政年份:2017
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负责人:Dihua Yu
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依托单位:
Inhibition of brain metastasis by blocking MAPK12 driver kinase functions
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资助金额:$55.25万
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Target p70S6K for Chemodietary Prevention/Early Intervention of ER- Breast Cancer
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Metabolic Deregulation by 14-3-3 in Mammary Tumor Progression
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PTEN Deficiency and Trastuzumab Resistance
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批准号:7737056
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资助金额:$18.13万
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财政年份:2008
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依托单位:
14-3-3zeta in ErbB2 Mediated Mammary Carcinogenesis
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Stromal activation in the progression of high ErbB2/1433zeta DCIS to IBC
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资助金额:$25.83万
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Stromal activation in the progression of high ErbB2/1433zeta DCIS to IBC
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14-3-3zeta in ErbB2 Mediated Mammary Carcinogenesis
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Stromal activation in the progression of high ErbB2/1433zeta DCIS to IBC
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项目类别:
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资助金额:$38.52万
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财政年份:2005
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依托单位:
海外基金