人人为我，我为FOSL1：FOSL1处于由突变KRAS驱动的肺癌和胰腺癌的交叉点。
All for one and FOSL1 for all: FOSL1 at the crossroads of lung and pancreatic cancer driven by mutant KRAS.
作者信息
Vallejo Adrian, Valencia Karmele, Vicent Silvestre
机构信息
Program in Solid Tumors and Biomarkers, Center for Applied Medical Research, Universidad de Navarra, Pamplona, Spain.
Department of Histology and Pathology, University of Navarra, Pamplona, Spain.
出版信息
Mol Cell Oncol. 2017 Apr 5;4(3):e1314239. doi: 10.1080/23723556.2017.1314239. eCollection 2017.
Abstract
() remains refractory to current therapies. We devised an integrative cross-tumor approach to expose common core elements up-regulated in mutant KRAS cancers that could provide new treatment opportunities. This approach identified () as a clinically and functionally relevant gene in mutant -driven lung and pancreatic cancers, and unveiled downstream transcriptional targets amenable to pharmacological inhibition.
摘要
（）对当前治疗方法仍具有难治性。我们设计了一种综合的跨肿瘤方法，以揭示在突变型KRAS癌症中上调的共同核心元件，这可能提供新的治疗机会。该方法确定（）为突变驱动的肺癌和胰腺癌中一个临床和功能相关的基因，并揭示了适合进行药物抑制的下游转录靶点。
相似文献
1
All for one and FOSL1 for all: FOSL1 at the crossroads of lung and pancreatic cancer driven by mutant KRAS.人人为我，我为FOSL1：FOSL1处于由突变KRAS驱动的肺癌和胰腺癌的交叉点。
Mol Cell Oncol. 2017 Apr 5;4(3):e1314239. doi: 10.1080/23723556.2017.1314239. eCollection 2017.
2
An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.综合分析揭示 FOSL1 是 KRAS 驱动的肺癌和胰腺癌的致癌基因脆弱性。
Nat Commun. 2017 Feb 21;8:14294. doi: 10.1038/ncomms14294.
3
FOSL1 promotes cholangiocarcinoma via transcriptional effectors that could be therapeutically targeted.FOSL1 通过可作为治疗靶点的转录效应因子促进胆管癌的发生。
J Hepatol. 2021 Aug;75(2):363-376. doi: 10.1016/j.jhep.2021.03.028. Epub 2021 Apr 20.
4
Inhibitor of Differentiation-1 Sustains Mutant -Driven Progression, Maintenance, and Metastasis of Lung Adenocarcinoma via Regulation of a FOSL1 Network.分化抑制因子 1 通过调节 FOSL1 网络维持肺腺癌的驱动突变、进展、维持和转移。
Cancer Res. 2019 Feb 1;79(3):625-638. doi: 10.1158/0008-5472.CAN-18-1479. Epub 2018 Dec 18.
5
An integrative pharmacogenomics analysis identifies therapeutic targets in KRAS-mutant lung cancer.综合药物基因组学分析鉴定 KRAS 突变型肺癌的治疗靶点。
EBioMedicine. 2019 Nov;49:106-117. doi: 10.1016/j.ebiom.2019.10.012. Epub 2019 Oct 23.
6
Epithelial-to-Mesenchymal Transition Defines Feedback Activation of Receptor Tyrosine Kinase Signaling Induced by MEK Inhibition in KRAS-Mutant Lung Cancer.上皮-间质转化定义了KRAS突变型肺癌中MEK抑制诱导的受体酪氨酸激酶信号的反馈激活。
Cancer Discov. 2016 Jul;6(7):754-69. doi: 10.1158/2159-8290.CD-15-1377. Epub 2016 May 6.
7
Excavation of FOSL1 in the Ruins of KRAS-Driven Lung Cancer.
Am J Respir Cell Mol Biol. 2018 May;58(5):551-552. doi: 10.1165/rcmb.2017-0369ED.
8
Co-dependency of PKCδ and K-Ras: inverse association with cytotoxic drug sensitivity in KRAS mutant lung cancer.蛋白激酶Cδ（PKCδ）与K-Ras的相互依赖：与KRAS突变型肺癌中细胞毒性药物敏感性呈负相关
Oncogene. 2017 Jul 27;36(30):4370-4378. doi: 10.1038/onc.2017.27. Epub 2017 Apr 3.
9
Mutant KRAS-driven cancers depend on PTPN11/SHP2 phosphatase.突变 KRAS 驱动的癌症依赖于 PTPN11/SHP2 磷酸酶。
Nat Med. 2018 Jul;24(7):954-960. doi: 10.1038/s41591-018-0024-8. Epub 2018 May 28.
10
Cigarette Smoke Induces Stem Cell Features of Pancreatic Cancer Cells via PAF1.香烟烟雾通过 PAF1 诱导胰腺癌干细胞特征
Gastroenterology. 2018 Sep;155(3):892-908.e6. doi: 10.1053/j.gastro.2018.05.041. Epub 2018 Jun 2.
引用本文的文献
1
ALKBH5 promotes the progression of infantile hemangioma through regulating the NEAT1/miR-378b/FOSL1 axis.ALKBH5 通过调控 NEAT1/miR-378b/FOSL1 轴促进婴幼儿血管瘤的进展。
Mol Cell Biochem. 2022 May;477(5):1527-1540. doi: 10.1007/s11010-022-04388-2. Epub 2022 Feb 18.
2
Signaling levels mold the RAS mutation tropism of urethane.信号水平塑造了氨基甲酸乙酯的 RAS 突变倾向。
Elife. 2021 May 17;10:e67172. doi: 10.7554/eLife.67172.
3
Gene signature for prognosis in comparison of pancreatic cancer patients with diabetes and non-diabetes.胰腺癌合并糖尿病与非糖尿病患者预后的基因特征比较
PeerJ. 2020 Nov 11;8:e10297. doi: 10.7717/peerj.10297. eCollection 2020.
4
Evolutionarily novel genes are expressed in transgenic fish tumors and their orthologs are involved in development of progressive traits in humans.进化上的新基因在转基因鱼肿瘤中表达，并且它们的直系同源基因与人类渐进性特征的发展有关。
Infect Agent Cancer. 2019 Dec 5;14:46. doi: 10.1186/s13027-019-0262-5. eCollection 2019.
5
Transcription factor 7 promotes the progression of perihilar cholangiocarcinoma by inducing the transcription of c-Myc and FOS-like antigen 1.转录因子 7 通过诱导 c-Myc 和 FOS 样抗原 1 的转录促进肝门部胆管癌的进展。
EBioMedicine. 2019 Jul;45:181-191. doi: 10.1016/j.ebiom.2019.06.023. Epub 2019 Jun 24.
本文引用的文献
1
An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.综合分析揭示 FOSL1 是 KRAS 驱动的肺癌和胰腺癌的致癌基因脆弱性。
Nat Commun. 2017 Feb 21;8:14294. doi: 10.1038/ncomms14294.
2
miR-1298 Inhibits Mutant KRAS-Driven Tumor Growth by Repressing FAK and LAMB3.miR-1298通过抑制粘着斑激酶（FAK）和层粘连蛋白β3（LAMB3）来抑制突变型KRAS驱动的肿瘤生长。
Cancer Res. 2016 Oct 1;76(19):5777-5787. doi: 10.1158/0008-5472.CAN-15-2936.
3
RAS Synthetic Lethal Screens Revisited: Still Seeking the Elusive Prize?重新审视RAS合成致死筛选：仍在追寻难以捉摸的目标？
Clin Cancer Res. 2015 Apr 15;21(8):1802-9. doi: 10.1158/1078-0432.CCR-14-2180.
4
Dragging ras back in the ring.将 ras 拖回拳击场。
Cancer Cell. 2014 Mar 17;25(3):272-81. doi: 10.1016/j.ccr.2014.02.017.
5
Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies.鉴定 KRAS 癌基因依赖性肿瘤细胞中的合成致死相互作用，揭示了新的治疗靶标策略。
Cell Res. 2012 Aug;22(8):1227-45. doi: 10.1038/cr.2012.82. Epub 2012 May 22.
6
A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene.一项全基因组RNA干扰筛选鉴定出了与Ras癌基因的多种合成致死相互作用。
Cell. 2009 May 29;137(5):835-48. doi: 10.1016/j.cell.2009.05.006.
7
FRA1 is a determinant for the difference in RAS-induced transformation between human and rat fibroblasts.FRA1是人类和大鼠成纤维细胞中RAS诱导转化差异的一个决定因素。
Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5490-5. doi: 10.1073/pnas.0601222103. Epub 2006 Mar 28.
8
ERK-MAPK signaling coordinately regulates activity of Rac1 and RhoA for tumor cell motility.ERK-MAPK信号传导协同调节Rac1和RhoA的活性以促进肿瘤细胞迁移。
Cancer Cell. 2003 Jul;4(1):67-79. doi: 10.1016/s1535-6108(03)00162-4.
9
Transformation by ras modifies AP1 composition and activity.
Oncogene. 1997 Feb 20;14(7):837-47. doi: 10.1038/sj.onc.1200900.
Zotero 插件