ArticlePLoS computational biology2021
The landscape of metabolic pathway dependencies in cancer cell lines.
Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- UPP1 in Cancer: Context-Dependent Roles in Metabolic Adaptation and Treatment Response.Current issues in molecular biology · 2026Review
- Cellular metabolomics reveals the osteogenic mechanism of MC3T3-E1 cells in porous Ti6Al4V scaffolds under low-intensity pulsed ultrasound.Frontiers in cell and developmental biology · 2026Article
- Review
- Spatial Immunometabolism: Integrating Technologies to Decode Cellular Metabolism in Tissues.European journal of immunology · 2025Review
- Luminescence Fingerprint of Intracellular NIR-II Gold Nanocluster Transformation: Implications for Sensing and Imaging.ACS nano · 2025Article
- Orchestrated desaturation reprogramming from stearoyl-CoA desaturase to fatty acid desaturase 2 in cancer epithelial-mesenchymal transition and metastasis.Cancer communications (London, England) · 2025Article
- Unveiling prognostic value of JAK/STAT signaling pathway related genes in colorectal cancer: a study of Mendelian randomization analysis.Infectious agents and cancer · 2025Article
- Multivariate analysis of metabolic state vulnerabilities across diverse cancer contexts reveals synthetically lethal associations.Cell reports · 2024Article
- Multivariate analysis of metabolic state vulnerabilities across diverse cancer contexts reveals synthetically lethal associations.bioRxiv : the preprint server for biology · 2024Article
- Metabolic profiling reveals metabolic features of consolidation therapy in pediatric acute lymphoblastic leukemia.Cancer & metabolism · 2023Article
- Identifying essential genes in genome-scale metabolic models of consensus molecular subtypes of colorectal cancer.PloS one · 2023Article
- Metabolomics paves the way for improved drug target identification.Molecular systems biology · 2022Article
- A Resource to Infer Molecular Paths Linking Cancer Mutations to Perturbation of Cell Metabolism.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The metabolic reprogramming of cancer cells creates metabolic vulnerabilities that can be therapeutically targeted. However, our understanding of metabolic dependencies and the pathway crosstalk that creates these vulnerabilities in cancer cells remains incomplete. Here, by integrating gene expression data with genetic loss-of-function and pharmacological screening data from hundreds of cancer cell lines, we identified metabolic vulnerabilities at the level of pathways rather than individual genes. This approach revealed that metabolic pathway dependencies are highly context-specific such that cancer cells are vulnerable to inhibition of one metabolic pathway only when activity of another metabolic pathway is altered. Notably, we also found that the no single metabolic pathway was universally essential, suggesting that cancer cells are not invariably dependent on any metabolic pathway. In addition, we confirmed that cell culture medium is a major confounding factor for the analysis of metabolic pathway vulnerabilities. Nevertheless, we found robust associations between metabolic pathway activity and sensitivity to clinically approved drugs that were independent of cell culture medium. Lastly, we used parallel integration of pharmacological and genetic dependency data to confidently identify metabolic pathway vulnerabilities. Taken together, this study serves as a comprehensive characterization of the landscape of metabolic pathway vulnerabilities in cancer cell lines.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.