Killing Tumors by Keeping Ras and PI3′ Kinase Apart
Open accessAbstract
Ras proteins mediate PI3K activation through direct binding to p110 catalytic subunits. However, it is unclear when and where this interaction occurs. In this issue of Cancer Cell, Castellano and colleagues report that KRAS-driven lung cancers require the Ras-p110α interaction for full activation of PI3K and tumor maintenance.
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The IGF1R/ERBB2/3 signaling pathway may respond to the suppressed ERK and AKT signaling after KRAS (G12C) inhibitor treatment and favor the change to epithelial cell types.
“The IGF1R/ERBB2/3 signaling pathway may respond to the suppressed ERK and AKT signaling after KRAS (G12C) inhibitor treatment and favor the change to epithelial cell types (Fig. 5).”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [134]
This changed cell type is more sensitive to co-inhibition by SHP2 and SOS1.
“This changed cell type is more sensitive to co-inhibition by SHP2 and SOS1 [130–135].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [134]
High basal ERBB2/3 associated with epithelial gene signatures was observed in KRAS (G12C) cell lines and human lung cancers.
“High basal ERBB2/3 associated with epithelial gene signatures was observed in KRAS (G12C) cell lines and human lung cancers.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [134]
Cites
Crystal Structure and Functional Analysis of Ras Binding to Its Effector Phosphoinositide 3-Kinase γ
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Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice
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Self-citationRAS and RHO Families of GTPases Directly Regulate Distinct Phosphoinositide 3-Kinase Isoforms
Fritsch, R., de Krijger, I., Fritsch, K., George, R., Reason, B., Kumar, M. S., Diefenbacher, M. E., Stamp, G., & Downward, J. (2013) · Cell · doi:10.1016/j.cell.2013.04.031 · Cited by 309 · see citing works
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Cooperative Activation of PI3K by Ras and Rho Family Small GTPases
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Requirement for Interaction of PI3-Kinase p110α with RAS in Lung Tumor Maintenance
Castellano, E., Sheridan, C., Thin, M. Z., Nye, E. L., Spencer‐Dene, B., Diefenbacher, M. E., Moore, C., Kumar, M. S., Murillo, M. M., Gronroos, E. C., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.09.012 · Cited by 184 · see citing works
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Defective K-Ras oncoproteins overcome impaired effector activation to initiate leukemia in vivo
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Adachi, Y., Ito, K., Hayashi, Y., Kimura, R., Tan, T. Z., Yamaguchi, R., & Ebi, H. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-2077 · Cited by 249 · see citing works
Targeting KRAS mutant cancers: from druggable therapy to drug resistance
Zhu, C., Guan, X., Zhang, X., Luan, X., Song, Z., Cheng, X., Zhang, W., & Qin, J.-J. (2022) · Molecular Cancer · doi:10.1186/s12943-022-01629-2 · Cited by 231 · see citing works
Vasjari, L., Bresan, S., Biskup, C. U., Pai, G. M., & Rubio, I. (2018) · Cell Cycle · doi:10.1080/15384101.2018.1560205 · Cited by 38 · see citing works
The Potential Treatment Options and Combination Strategies of KRAS-Mutated Lung Cancer
Zhao, X., Zheng, Y., Wang, Y., Zhang, M., Dong, Z., Liu, Y., & Sun, M. (2024) · OncoTargets and Therapy · doi:10.2147/ott.s484209 · Cited by 4 · see citing works
Malek, S., & McCormick, F. P. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.02001-5
Self-citation
- Authors
- Yuan, T. L., & McCormick, F.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- McCormick, Frank
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 24
- Issue
- 5
- Pages
- 562-563
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2025653961
- Cited by
- 5
- References
- 10
- Citations by year
- 2024: 2 · 2022: 1 · 2020: 1 · 2018: 1
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (T32CA108462)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- Ras, phosphatidylinositol 3-kinase, p110α, KRAS, lung cancer, PI3K activation, tumor maintenance, oncogenic signaling
- MeSH terms
- Adenocarcinoma, Animals, Humans, Lung Neoplasms, Proto-Oncogene Proteins p21(ras), Class I Phosphatidylinositol 3-Kinases
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