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Oncogenic Kras Maintains Pancreatic Tumors through Regulation of Anabolic Glucose Metabolism
Open accessAbstract
Tumor maintenance relies on continued activity of driver oncogenes, although their rate-limiting role is highly context dependent. Oncogenic Kras mutation is the signature event in pancreatic ductal adenocarcinoma (PDAC), serving a critical role in tumor initiation. Here, an inducible Kras(G12D)-driven PDAC mouse model establishes that advanced PDAC remains strictly dependent on Kras(G12D) expression. Transcriptome and metabolomic analyses indicate that Kras(G12D) serves a vital role in controlling tumor metabolism through stimulation of glucose uptake and channeling of glucose intermediates into the hexosamine biosynthesis and pentose phosphate pathways (PPP). These studies also reveal that oncogenic Kras promotes ribose biogenesis. Unlike canonical models, we demonstrate that Kras(G12D) drives glycolysis intermediates into the nonoxidative PPP, thereby decoupling ribose biogenesis from NADP/NADPH-mediated redox control. Together, this work provides in vivo mechanistic insights into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit in PDAC.
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“Prior studies have demonstrated that genetic ablation of KRAS expression leads to cell cycle arrest and death in cell lines and potent tumor regressions in animal models of PDAC (5–7).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Consistent with our previous findings on the role of glycolysis as a critical downstream effector of oncogenic KRAS signaling in advanced tumors,16,17”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the iKras GEM model, acute extinction of mutant KRAS results in downregulation of SDC1 expression, coinciding with suppression of MAPK signaling, as evidenced by reduced ERK phosphorylation.12,17”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [17]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“KRAS mutations lead to sustained activation of MAPK and PI3K-mTOR pathways16,17”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [16]
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In the citing paper
“Pancreatic ductal adenocarcinoma (PDAC) lines were chosen for our study because cancers of the pancreas are characterized by rapid progression,9,10 invasiveness,11,12 and elevated fermentative metabolism.13,14,15,16”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [16]
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In the citing paper
“pancreatic cancers generate substantial lactic acid fluxes, linked to mutations that promote hyper-proliferation”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [16]
In the citing paper
“KRAS also promotes the hexosamine biosynthesis pathway (HBP), which provides precursors for lipid and protein glycosylation34, and the non-oxidative arm of the pentose phosphate pathway (PPP)28, which supplies ribose, the backbone for nucleic acid production35 (Fig 2).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [28]
In the citing paper
“KRAS regulates these pathways through MAPK-dependent signaling cascades, ultimately supporting cell survival and conferring a proliferative advantage on tumors28,36,37.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [28]
In the citing paper
“Oncogenic KRAS also upregulates expression of other key glycolytic enzymes, such as PFK1, ENO1, and LDHA28,31–33, thereby promoting glycolytic flux and enabling the production of glycolytic intermediates that can be shunted into other anabolic pathways (Fig 2).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [28]
In the citing paper
“Gene expression and metabolic flux analyses have shown that it upregulates the expression of the GLUT1 glucose transporter to promote glucose uptake by cells, as well as inducing expression of hexokinase 1 and 2 (HK1 and HK2) rate-limiting enzymes of glycolysis, to increase glycolytic activity27–30 (Fig. 2a).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [28]
In the citing paper
“Mouse PDAC tumors driven by mutant Kras also experience metabolic alteration and are dependent on glucose and glutamine (73, 77).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [73]
In the citing paper
“Extinguishing the expression of mutant Kras in the pancreas led to rapid tumor regression, thus demonstrating a critical role of Kras in tumor maintenance (73, 78).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [73]
In the citing paper
“Withdrawal of oncogenic Kras resulted in regression of invasive neoplasia, including regression of metastatic disease63–65.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [64]
In the citing paper
“Examples include the non-oxidative pentose phosphate pathway, which enables nucleotide biosynthesis, and the hexosamine biosynthesis pathway, which generates GlcNAc required for posttranslational modifications64,195”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [64]
In the citing paper
“Mutant KRAS drives upregulated glycolysis, not only increasing production of lactate, but also providing key carbon inputs for synthesis of molecules required for proliferation.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [64]
In the citing paper
“Thus, NRF2- mediated metabolic reprogramming and regulation of redox homeostasis likely underpin the strong co-selection of KEAP1 with LKB1 and KRAS mutations in NSCLC at least partially because oncogenic KRAS itself promotes oxidative stress and anabolic metabolism and because KL NSCLC cells depend on the pentose phosphate pathway for NAPDH generation and for detoxification of reactive oxygen”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [98]
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Metadata
- Authors
- Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., Yan, H., Wang, W., Chen, S., Viale, A., Zheng, H., Paik, J.-H., Lim, C., Guimaraes, A. R., Martin, E. S., Chang, J., Hezel, A. F., Perry, S. R., Hu, J., Gan, B., Xiao, Y., Asara, J. M., Weissleder, R., Wang, Y. A., Chin, L., Cantley, L. C., & DePinho, R. A.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Beth Israel Deaconess Medical Center (US)
- Brigham and Women's Hospital (US)
- Harvard University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Kimmelman, Alec C.
- DePinho, Ronald A.
- ORCID
- Ying, Haoqiang
- Kimmelman, Alec C.
- Lyssiotis, Costas A.
- Locasale, Jason W.
- Son, Jaekyoung
- Zhang, Hailei
- Coloff, Jonathan L.
- Yan, Haiyan
- Wang, Wei
- Chen, Shujuan
- Viale, Andrea
- Zheng, Hongwu
- Martin, Eric S.
- Hezel, Aram F.
- Hu, Jian
- Gan, Boyi
- Xiao, Yonghong
- Asara, John M.
- Weissleder, Ralph
- Wang, Y. Alan
- Cantley, Lewis C.
- DePinho, Ronald A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 149
- Issue
- 3
- Pages
- 656-670
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3472002
- OpenAlex
- W2069269337
- Cited by
- 2,043
- References
- 55
- Citations by year
- 2026: 139 · 2025: 129 · 2024: 154 · 2023: 175 · 2022: 178 · 2021: 200 · 2020: 153 · 2019: 164 · 2018: 135 · 2017: 153 · 2016: 139 · 2015: 114 · 2014: 105 · 2013: 79 · 2012: 23
- FWCI
- 50.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Cancer Institute (P50-CA-86355, U24CA092782, P50CA086355, T32CA009382, R01CA157490, P01CA120964, P01CA117969, P30CA006516)
- National Institute of General Medical Sciences (R01GM056203)
- National Institute of Biomedical Imaging and Bioengineering (K08EB012859)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- oncogenic KRAS, pancreatic ductal adenocarcinoma, tumor maintenance, glucose metabolism, metabolic reprogramming, hexosamine biosynthetic pathway, pentose phosphate pathway, glycolysis intermediates, cancer metabolism
- MeSH terms
- Adenocarcinoma, Animals, Disease Models, Animal, Humans, Pancreatic Neoplasms, Transcription, Genetic, Proto-Oncogene Proteins p21(ras), Mice
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