Survival of pancreatic cancer cells lacking KRAS function
Open accessAbstract
Activating mutations in the proto-oncogene KRAS are a hallmark of pancreatic ductal adenocarcinoma (PDAC), an aggressive malignancy with few effective therapeutic options. Despite efforts to develop KRAS-targeted drugs, the absolute dependence of PDAC cells on KRAS remains incompletely understood. Here we model complete KRAS inhibition using CRISPR/Cas-mediated genome editing and demonstrate that KRAS is dispensable in a subset of human and mouse PDAC cells. Remarkably, nearly all KRAS deficient cells exhibit phosphoinositide 3-kinase (PI3K)-dependent mitogen-activated protein kinase (MAPK) signaling and induced sensitivity to PI3K inhibitors. Furthermore, comparison of gene expression profiles of PDAC cells retaining or lacking KRAS reveal a role of KRAS in the suppression of metastasis-related genes. Collectively, these data underscore the potential for PDAC resistance to even the very best KRAS inhibitors and provide insights into mechanisms of response and resistance to KRAS inhibition.
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KRAS-independent survival was observed in some PDAC cells, with PI3K pathway playing compensatory role.
“Moreover, KRAS-independent survival was observed in some PDAC cells, with the PI3K pathway playing a compensatory role.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [92]
In some cases, complete ablation of KRAS gene using CRISPR-Cas9 does not affect cell viability in KRAS mutant models.
“In some cases, even complete ablation of KRAS gene using CRISPR-Cas9 technology does not affect cell viability in KRAS mutant models.63”
From Overcoming Resistance to Drugs Targeting KRAS Mutation (2020) · cites this paper as [63]
Redundancy of parallel growth signals could bypass the necessity of mutant K-Ras in promoting cell proliferation and underlies inherent resistance to K-RasG12C-targeted therapies.
“Therefore, the redundancy of parallel growth signals could bypass the necessity of mutant K-Ras in promoting cell proliferation and underlies the inherent resistance to K-RasG12C-targeted therapies (Figure 3A–3C).12,63”
From Overcoming Resistance to Drugs Targeting KRAS Mutation (2020) · cites this paper as [63]
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Rafael, D. F. D. S., Montero, S., Carcavilla, P., Andrade, F., German-Cortés, J., Díaz‐Riascos, Z. V., Seras‐Franzoso, J., Munive, M. L., Fernández, B., Pereira, A., et al. (2023) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.2c19897 · Cited by 13 · see citing works
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Complex interplay between RAS GTPases and RASSF effectors regulates subcellular localization of YAP
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- Authors
- Muzumdar, M. D., Chen, P.-Y., Dorans, K. J., Chung, K. M., Bhutkar, A., Hong, E., Noll, E. M., Sprick, M. R., Trumpp, A., & Jacks, T.
- Affiliations
- Harvard University (US)
- Koch Institute for Integrative Cancer Research At MIT (US)
- German Cancer Research Center (DE)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Jacks, Tyler
- ORCID
- Venue
- Nature Communications
- Published
- 2017-10-23
- Volume
- 8
- Issue
- 1
- Pages
- 1090-1090
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5653666
- OpenAlex
- W2765585947
- Cited by
- 177
- References
- 70
- Citations by year
- 2026: 10 · 2025: 17 · 2024: 20 · 2023: 19 · 2022: 23 · 2021: 30 · 2020: 19 · 2019: 21 · 2018: 16 · 2017: 2
- FWCI
- 6.99
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- Nature
- Funders
- U.S. Department of Defense (W81XWH-12-043, P30-CA14051, W81XWH, W81XWH-12)
- Howard Hughes Medical Institute (P30-CA14051)
- Conquer Cancer Foundation
- Pancreatic Cancer Action Network
- American Society of Clinical Oncology
- Harvard University (KL2 TR001100)
- Harvard Catalyst (KL2 TR001100, TR001100)
- Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology (P30-CA14051, Grant P30-CA14051)
- National Institutes of Health (W81XWH, KL2TR001100)
- National Cancer Institute (K08CA208016, CA14051, K08-CA2080016, U01CA199253, Grant P30-CA14051, P30CA014051, P30-CA-14051)
- National Center for Research Resources
- National Center for Advancing Translational Sciences (TR001100)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- pancreatic ductal adenocarcinoma, KRAS, KRAS inhibition, PI3K signaling, MAPK signaling, PI3K inhibitors, drug resistance, metastasis-associated genes, gene expression profiling, CRISPR/Cas genome editing
- MeSH terms
- Proto-Oncogene Mas, Animals, Antineoplastic Agents, Benzimidazoles, Humans, Indazoles, Morpholines, Pancreatic Neoplasms, Phenylurea Compounds, Piperidines, Purines, Pyrimidines, Pyrimidinones, Sulfonamides, Thiazoles, Immunoblotting, Proto-Oncogene Proteins p21(ras), Carcinoma, Pancreatic Ductal, Mice, Quinazolinones, DNA Copy Number Variations
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