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Protein Kinase Cι Drives a NOTCH3-dependent Stem-like Phenotype in Mutant KRAS Lung Adenocarcinoma
Cancer Cell, Issue: 3, Volume: 29, Pages: 367-378. | 2016-01-03
0 Patent citations    14 Scholarly citations     Reference Count: 64
Syed A Ali;Verline Justilien;Lee Jamieson;Nicole R Murray;Alan P Fields

摘要

Summary We report that the protein kinase Cι (PKCι) oncogene controls expression of NOTCH3, a key driver of stemness, in KRAS -mediated lung adenocarcinoma (LADC). PKCι activates NOTCH3 expression by phosphorylating the ELF3 transcription factor and driving ELF3 occupancy on the NOTCH3 promoter. PKCι-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 PKCι-ELF3-NOTCH3 signaling, and combined pharmacologic blockade of PKCι and NOTCH synergistically inhibits tumorigenic behavior in vitro and LADC growth in vivo demonstrating the therapeutic potential of PKCι-ELF3-NOTCH3 signal inhibition to more effectively treat KRAS LADC.


机构

Mayo Clinic;Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA.Mayo Clinic;Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA.Mayo Clinic;Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA.Mayo Clinic;Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA.Mayo Clinic;Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA. Electronic address: fields.alan@mayo.edu.


文献类型:

journal article;research support, n.i.h., extramural;research support, non-u.s. gov't;

出版商:

Cell Press

发表时间:

2016-01-03

基金信息

NCI NIH HHS(R21 CA151250)United States