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ABSTRACT
We have recently demonstrated that protein kinase Cι (PKCι) promotes a stem-like, tumor-initiating cell phenotype in KRAS-driven lung adenocarcinoma by activating a novel ELF3-NOTCH3 signaling axis.Citation1 Combined PKCι and NOTCH inhibition was identified as a novel strategy for the treatment of KRAS-driven lung adenocarcinoma.
Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
Acknowledgments
The work described herein was supported by grants from the National Institutes of Health (R01 CA081436-17 and R21 CA151250-02 to APF; R01 CA14090-05 to NRM; and R21 CA204938-01 (VJ); the James and Esther King Biomedical Research Program (1KG-05-33971) to APF, the Mayo Clinic Center for Individualized Medicine (CIM) to APF; a National Institutes of Health Research Supplement to Promote Diversity in Health-related Research Award from the National Cancer Institute to VJ, and the George Haub Family Career Development Award (VJ). APF is the Monica Flynn Jacoby Professor of Cancer Research. SAA is the recipient of the Edward C. Kendall Fellowship in Biochemistry from the Mayo Clinic Graduate School.