ZEB1 suppression sensitizes KRAS mutant cancers to MEK inhibition by an IL17RD-dependent mechanism
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Suppression of ZEB1 through miR-200 expression or HDAC inhibition with mocetinostat sensitizes resistant KRAS mutant lung cancers to MEK inhibition.
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Strategies that reverse EMT and co-target FGFR and IGFR signaling could re-sensitize EMT-induced cells to KRAS and MEK inhibitors.
“Strategies that reverse the EMT transcriptional program, as well as co-targeting FGFR and IGFR signaling in EMT-induced cells could re-sensitize them towards KRAS and MEK inhibitors (46, 47)”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [46]
In mesenchymal-like KRAS-mutant lung cancer cells, ZEB1 directly represses IL17RD to mediate resistance to MEK inhibitors.
“in mesenchymal-like KRAS-mutant lung cancer cells, ZEB1 directly represses IL17RD to mediate the resistance to MEK inhibitors.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [28]
MAPK dependency is dictated by the functional interplay between IL17RD and ZEB1.
“Mechanistic results indicated that MAPK dependency is dictated by the functional interplay between scaffold protein interleukin-17 receptor D (IL17RD) and ZEB1.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [28]
ZEB1 suppression by miR-200 expression or mocetinostat re-sensitized mesenchymal cells to MEK inhibition and markedly reduced in vivo tumor growth.
“ZEB1 suppression by miR-200 expression or histone deacetylase inhibitor (mocetinostat) re-sensitized mesenchymal cells to MEK inhibition and markedly reduced in vivo tumor growth.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [28]
Peng et al. identified an inverse correlation between MAPK signaling dependency and ZEB1-mediated EMT in patient samples harboring KRAS, BRAF, or NRAS mutations.
“Peng et al. identified an inverse correlation between MAPK signaling dependency and a zinc finger E-box binding homeobox 1 (ZEB1)–mediated EMT in patient samples harboring KRAS, BRAF, or NRAS mutations.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [28]
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- Authors
- Peng, D. H., Kundu, S. T., Fradette, J. J., Diao, L., Tong, P., Byers, L. A., Wang, J., Canales, J. R., Villalobos, P. A., Mino, B., Yang, Y., Minelli, R., Peoples, M. D., Bristow, C. A., Heffernan, T. P., Carugo, A., Wistuba, I. I., & Gibbons, D. L.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Mayo Clinic (US)
- Corresponding author
- Gibbons, Don L.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2019-03-13
- Volume
- 11
- Issue
- 483
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6878763
- OpenAlex
- W2922513518
- Cited by
- 53
- References
- 61
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 13 · 2020: 9 · 2019: 6
- FWCI
- 2.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P50CA070907, R37CA214609, P30CA016672)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- ZEB1, KRAS mutation, MEK inhibitors, MAPK signaling, lung cancer, drug sensitivity, predictive biomarkers, transcriptional repression
- MeSH terms
- Zinc Finger E-box-Binding Homeobox 1, Animals, Benzamides, Disease Models, Animal, Epithelial Cells, Humans, Lung Neoplasms, Mesoderm, Mutation, Neoplasms, Phosphorylation, Pyrimidines, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, Mitogen-Activated Protein Kinase Kinases, MAP Kinase Signaling System, MicroRNAs, Cell Line, Tumor, Protein Kinase Inhibitors, Cell Proliferation, Mice, Receptors, Interleukin-17
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