mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability

Valvezan AJ, Turner M, Belaid A, Lam HC, Miller SK, McNamara MC, Baglini C, Housden BE, Perrimon N, Kwiatkowski DJ, Asara JM, …, Manning BD · 2017 · Cancer cell · Atlas ID VAL2017

What this study shows

Hyperactive mTORC1 couples nucleotide synthesis to demand; imbalance drives replication stress in these cells.

Abstract

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The mechanistic target of rapamycin complex 1 (mTORC1) supports proliferation through parallel induction of key anabolic processes, including protein, lipid, and nucleotide synthesis. We hypothesized that these processes are coupled to maintain anabolic balance in cells with mTORC1 activation, a common event in human cancers. Loss of the tuberous sclerosis complex (TSC) tumor suppressors results in activation of mTORC1 and development of the tumor syndrome TSC.

Read the full abstract on PubMed →

At a glance

Evidence type	M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Cancer cells; tumor) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is.
Study type	5 - Mechanistic / In Vitro
Model system	Cancer cells; tumor
Journal	Cancer cell
Year	2017
Peer reviewed	Yes
Record last updated	2026-07-29
Source	DOI 10.1016/j.ccell.2017.09.013 · PMID 29056426 · Free full text (PMC5687294)

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	Genetic/pharmacologic (mTORC1; TSC loss)
Target	mTORC1 / nucleotide synthesis
Model	Cancer cells; tumor
Effect	mTORC1 couples nucleotide synthesis to demand, creating a targetable metabolic vulnerability in TSC-null cancer

In the Atlas

Links in the pathway map

Supports mTORC1 activates Nucleotide synthesis
Supports mTORC1 activates Tumor growth

Cite this paper

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Valvezan, A. J., Turner, M., Belaid, A., Lam, H. C., Miller, S. K., McNamara, M. C., Baglini, C., Housden, B. E., Perrimon, N., Kwiatkowski, D. J., Asara, J. M., Henske, E. P., & Manning, B. D. (2017). mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability. Cancer cell. https://doi.org/10.1016/j.ccell.2017.09.013

@article{VAL2017,
  author       = {Valvezan, A. J. and Turner, M. and Belaid, A. and Lam, H. C. and Miller, S. K. and McNamara, M. C. and Baglini, C. and Housden, B. E. and Perrimon, N. and Kwiatkowski, D. J. and Asara, J. M. and Henske, E. P. and Manning, B. D.},
  title        = {{mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability}},
  journal      = {Cancer cell},
  year         = {2017},
  doi          = {10.1016/j.ccell.2017.09.013},
  note         = {PMID: 29056426},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record VAL2017) [Data set]. https://mtor-atlas.org/study/VAL2017/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_VAL2017,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record VAL2017},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/VAL2017/},
  doi          = {10.5281/zenodo.22059963}
}

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