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Peer-reviewedCC BYCellular and molecular life sciences : CMLS

Lung cancer metabolism: a dynamic and adaptive network.

  • Sara Gholamhosseinian-Najjar1
  • Christian Frezza2,3,4
4 affiliations
  1. 1Institute for Metabolomics in Ageing, Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
  2. 2Institute for Metabolomics in Ageing, Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany. [email protected].
  3. 3Institute of Genetics, Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), Faculty of Mathematics and Natural Sciences, University of Cologne, Cologne, Germany. [email protected].
  4. 4Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany. [email protected].
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Abstract

Lung cancer remains the leading cause of cancer-related mortality worldwide. Although substantial progress has been made in defining the genetic, epigenetic, and molecular drivers of this heterogeneous disease, metabolic reprogramming has only recently emerged as a major determinant of tumour progression and therapeutic response. Cumulative evidence demonstrates that rather than relying on a single nutrient source or pathway, cancer cells integrate glucose and glutamine, fatty acid and one-carbon metabolism, as well as nucleotide biosynthesis, and redox-supporting circuits in a highly context-dependent manner. These programs vary across histological and molecular subtypes, reflecting the influence of lineage identity and oncogenic state on metabolic organisation. In both non-small cell lung cancer and small cell lung cancer, subtype-specific constraints shape distinct metabolic states, yet a common feature is the ability to rapidly shift between alternative nutrients and biosynthetic routes. This adaptability supports continued growth under nutrient limitation, maintains redox homeostasis, and contributes to resistance against conventional and targeted therapies. By summarising current mechanistic evidence, this review presents lung cancer metabolism as an integrated and adaptable system rather than a collection of isolated pathways, and identifies metabolic dependencies that may be leveraged for therapeutic intervention.

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Cite

BibTeXRIS
BibTeX
@article{gholamhosseiniannajjar2026lung,
  title = {{Lung cancer metabolism: a dynamic and adaptive network.}},
  author = {Sara Gholamhosseinian-Najjar and Christian Frezza},
  journal = {Cellular and molecular life sciences : CMLS},
  year = {2026},
  month = oct,
  doi = {10.1007/s00018-026-06417-5},
  url = {https://europepmc.org/article/MED/42911237},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Lung cancer metabolism: a dynamic and adaptive network.
AU  - Sara Gholamhosseinian-Najjar
AU  - Christian Frezza
PY  - 2026
DA  - 2026/10/19
JO  - Cellular and molecular life sciences : CMLS
DO  - 10.1007/s00018-026-06417-5
UR  - https://europepmc.org/article/MED/42911237
AB  - Lung cancer remains the leading cause of cancer-related mortality worldwide. Although substantial progress has been made in defining the genetic, epigenetic, and molecular drivers of this heterogeneous disease, metabolic reprogramming has only recently emerged as a major determinant of tumour progression and therapeutic response. Cumulative evidence demonstrates that rather than relying on a single nutrient source or pathway, cancer cells integrate glucose and glutamine, fatty acid and one-carbon metabolism, as well as nucleotide biosynthesis, and redox-supporting circuits in a highly context-dependent manner. These programs vary across histological and molecular subtypes, reflecting the influence of lineage identity and oncogenic state on metabolic organisation. In both non-small cell lung cancer and small cell lung cancer, subtype-specific constraints shape distinct metabolic states, yet a common feature is the ability to rapidly shift between alternative nutrients and biosynthetic routes. This adaptability supports continued growth under nutrient limitation, maintains redox homeostasis, and contributes to resistance against conventional and targeted therapies. By summarising current mechanistic evidence, this review presents lung cancer metabolism as an integrated and adaptable system rather than a collection of isolated pathways, and identifies metabolic dependencies that may be leveraged for therapeutic intervention.
SN  - 1420-682X
SN  - 1420-9071
ER  -