Protein Kinase C iota Drives a NOTCH3-dependent Stem-like Phenotype in Mutant KRAS Lung Adenocarcinoma

Ali Syed A.; Justilien Verline; Jamieson Lee; Murray Nicole R.; Fields Alan P.

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Protein Kinase C iota Drives a NOTCH3-dependent Stem-like Phenotype in Mutant KRAS Lung Adenocarcinoma

机译：蛋白激酶C IOTA在突变体KRAS肺腺癌中驱动Notch3依赖性干燥表型

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We report that the protein kinase C iota (PKC iota) oncogene controls expression of NOTCH3, a key driver of stemness, in KRAS-mediated lung adenocarcinoma (LADC). PKC iota activates NOTCH3 expression by phosphorylating the ELF3 transcription factor and driving ELF3 occupancy on the NOTCH3 promoter. PKC iota-ELF3-NOTCH3 signaling controls the tumor-initiating cell phenotype by regulating asymmetric cell division, a process necessary for tumor initiation and maintenance. Primary LADC tumors exhibit PKC iota-ELF3-NOTCH3 signaling, and combined pharmacologic blockade of PKC iota and NOTCH synergistically inhibits tumorigenic behavior in vitro and LADC growth in vivo demonstrating the therapeutic potential of PKC iota-ELF3-NOTCH3 signal inhibition to more effectively treat KRAS LADC.

机译：我们认为蛋白激酶C IOTA（PKC IOTA）癌基因对kRas介导的肺腺癌（LADC）中的Notch3，茎的关键驱动器的表达。 PKC IOTA通过磷酸化ELF3转录因子并在Notch3启动子上驾驶ELF3占用来激活Notch3表达。 PKC IOTA-ELF3-NOTCH3信号传导通过调节不对称细胞分裂来控制肿瘤起始细胞表型，该方法是肿瘤起始和维护所需的方法。主要LADC肿瘤表现出PKC IOTA-ELF3-NOTCH3信号传导，PKC IOTA和NOTCH的组合药理学阻滞协同抑制体外致致瘤性行为和LADC生长的体内，证明了PKC IOTA-ELF3-Notch3信号抑制的治疗潜力更有效地治疗KRA Ladc。

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《Cancer Cell》 |2016年第3期|共12页
作者
Ali Syed A.; Justilien Verline; Jamieson Lee; Murray Nicole R.; Fields Alan P.;
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Mayo Clin Ctr Canc Dept Canc Biol Jacksonville FL 32224 USA;

Mayo Clin Ctr Canc Dept Canc Biol Jacksonville FL 32224 USA;

Mayo Clin Ctr Canc Dept Canc Biol Jacksonville FL 32224 USA;

Mayo Clin Ctr Canc Dept Canc Biol Jacksonville FL 32224 USA;

Mayo Clin Ctr Canc Dept Canc Biol Jacksonville FL 32224 USA;

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正文语种 eng
中图分类肿瘤学;
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1. Protein Kinase C iota Drives a NOTCH3-dependent Stem-like Phenotype in Mutant KRAS Lung Adenocarcinoma [J] . Ali Syed A., Justilien Verline, Jamieson Lee, Cancer Cell . 2016,第3期

机译：蛋白激酶C IOTA在突变体KRAS肺腺癌中驱动Notch3依赖性干燥表型
2. Osteopontin drives KRAS-mutant lung adenocarcinoma [J] . Giopanou Ioanna, Kanellakis Nikolaos I, Giannou Anastasios D., Carcinogenesis . 2020,第8期

机译：Osteopontin驱动Kras-突变体肺腺癌
3. I kappa B Kinase alpha Is Required for Development and Progression of KRAS-Mutant Lung Adenocarcinoma [J] . Vreka Malamati, Lilis Ioannis, Papageorgopoulou Maria, Cancer research: The official organ of the American Association for Cancer Research, Inc . 2018,第11期

机译：kappa b激酶α是kras-突变体肺腺癌的开发和进展所必需的
4. Bioinformatics analysis the hub-proteins and co-expression proteins of lung squamous carcinoma and adenocarcinoma based on protein interaction network [C] . Chen Qi-long, Qiao Zi-jun, Yang He-jian, 2011 IEEE International Conference on Computer Science and Automation Engineering . 2011

机译：基于蛋白质相互作用网络的生物信息学分析肺鳞癌和腺癌的枢纽蛋白和共表达蛋白
5. Role of Oncogenic Protein Kinase C-iota in Melanoma Progression; A Study Based on Atypical Protein Kinase-C Inhibitors [D] . Ratnayake, Wishrawana Sarathi Bandara. 2019

机译：致癌蛋白激酶C-IOTA在黑色素瘤进展中的作用; 基于非典型蛋白激酶-C抑制剂的研究
6. Protein Kinase Cι drives a NOTCH3-dependent stem-like phenotype in mutant KRAS lung adenocarcinoma [O] . Syed A. Ali, Verline Justilien, Lee Jamieson, -1

机译：蛋白激酶C1驱动突变型KRAS肺腺癌中NOTCH3依赖的干样表型
7. Protein Kinase Cι and Wnt/β-Catenin Signaling: Alternative Pathways to Kras/Trp53-Driven Lung Adenocarcinoma [O] . Ning Yin, Yi Liu, Andras Khoor, 2019

机译：蛋白激酶C1和Wnt /β-catenin信号传导：KRAS / TRP53驱动肺腺癌的替代途径

Protein Kinase C iota Drives a NOTCH3-dependent Stem-like Phenotype in Mutant KRAS Lung Adenocarcinoma

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