Evidence map›Paper›PMID 23475953›Full record

ArticleMolecular cancer research : MCR2013

Metabolic alterations in lung cancer-associated fibroblasts correlated with increased glycolytic metabolism of the tumor.

Virendra K Chaudhri, Gregory G Salzler, Salihah A Dick, Melanie S Buckman, Raffaella Sordella, Edward D Karoly, Robert Mohney, Brendon M Stiles, Olivier Elemento, Nasser K Altorki and 1 more

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed.

  1. Review
  2. Article
  3. Targeting CAF-specific metabolic pathways in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. A perspective on the role of autophagy in cancer.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Inflammation-Induced Tumorigenesis and Metastasis.International journal of molecular sciences · 2021
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Virendra K ChaudhriDepartment of Biochemistry, Weill Cornell Medical College New York, New York, NY 10065, USA.
Gregory G Salzler
Salihah A Dick
Melanie S Buckman
Raffaella Sordella
Edward D Karoly
Robert Mohney
Brendon M Stiles
Olivier Elemento
Nasser K Altorki
Timothy E McGraw

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Rebecca Anne Haeusler, Utpal Pajvani · 2003 to 2026
$36.7M
Clinical and Translational Science CenterTL1TR000459 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$451k
QUANTIMET 900 IMAGE ANALYSING SYSTEMS10RR002499 · NCRR · YESHIVA UNIVERSITY · PI BROWN, LUCY L · 1985 to 1985
–
NCATS NIH HHS TL1 TR000459NCATS NIH HHS UL1 TR000457NCRR NIH HHS TL1RR02499NIDDK NIH HHS DIRC P30DK063608-09NIDDK NIH HHS P30 DK063608NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Cancer cells undergo a metabolic reprogramming but little is known about metabolic alterations of other cells within tumors. We use mass spectrometry-based profiling and a metabolic pathway-based systems analysis to compare 21 primary human lung cancer-associated fibroblast lines (CAF) to "normal" fibroblast lines (NF) generated from adjacent nonneoplastic lung tissue. CAFs are protumorigenic, although the mechanisms by which CAFs support tumors have not been elucidated. We have identified several pathways whose metabolite abundance globally distinguished CAFs from NFs, suggesting that metabolic alterations are not limited to cancer cells. In addition, we found metabolic differences between CAFs from high and low glycolytic tumors that might reflect distinct roles of CAFs related to the tumor's glycolytic capacity. One such change was an increase of dipeptides in CAFs. Dipeptides primarily arise from the breakdown of proteins. We found in CAFs an increase in basal macroautophagy which likely accounts for the increase in dipeptides. Furthermore, we show a difference between CAFs and NFs in the induction of autophagy promoted by reduced glucose. In sum, our data suggest that increased autophagy may account for metabolic differences between CAFs and NFs and may play additional as yet undetermined roles in lung cancer.

Indexed as

GlycolysisAutophagyCell Line, TransformedCell SeparationFibroblastsGlucoseHumansLung NeoplasmsMetabolomicsMicrotubule-Associated ProteinsGlucoseMAP1LC3A protein, humanMicrotubule-Associated Proteins

Identifiers

PMID23475953
PMCPMC3686965

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Registered trials

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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.