Evidence map›Paper›PMID 22339657›Full record

ReviewCritical reviews in eukaryotic gene expression2012

Carbon source metabolism and its regulation in cancer cells.

Chengqian Yin, Shuo Qie, Nianli Sang

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in eukaryotic gene expression, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. LOC101929709 promotes gastric cancer progression by aiding LIN28B to stabilize c-MYC mRNA.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  10. Article
  11. Stanniocalcin 2 (STC2): a universal tumour biomarker and a potential therapeutical target.Journal of experimental & clinical cancer research : CR · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Chengqian YinDepartment of Biology, College of Arts and Sciences, Drexel University, Philadelphia, Pennsylvania, USA.
Shuo Qie
Nianli Sang
Drexel University · US

Funding

Repressing HIF-1: targets and mechanismsR01CA129494 · NCI · DREXEL UNIVERSITY · PI SANG, NIANLI · 2008 to 2012
$1.6M
NCI NIH HHS R01 CA129494NCI NIH HHS R01CA129494
6 · The paper itself

Abstract

Cancer cell proliferation and progression require sufficient supplies of nutrients including carbon sources, nitrogen sources, and molecular oxygen. Particularly, carbon sources and molecular oxygen are critical for the generation of ATP and building blocks, and for the maintenance of intracellular redox status. However, solid tumors frequently outgrow the blood supply, resulting in nutrient insufficiency. Accordingly, cancer cell metabolism shows aberrant biochemical features that are consequences of oncogenic signaling and adaptation. Those adaptive metabolism features, including the Warburg effect and addiction to glutamine, may form the biochemical basis for resistance to chemotherapy and radiation. A better understanding of the regulatory mechanisms that link the signaling pathways to adaptive metabolic reprogramming may identify novel biomarkers for drug development. In this review, we focus on the regulation of carbon source utilization at a cellular level, emphasizing its relevance to proliferative biosynthesis in cancer cells. We summarize the essential needs of proliferating cells and the metabolic features of glucose, lipids, and glutamine, and we review the roles of transcription regulators (i.e., HIF-1, c-Myc, and p53) and two major oncogenic signaling pathways (i.e., PI3K-Akt and MAPK) in regulating the utilization of carbon sources. Finally, the effects of glucose on cell proliferation and perspective from both biochemical and cellular angles are discussed.

Indexed as

Biomarkers, TumorAdenosine TriphosphateCarbonCell ProliferationEnergy MetabolismGene Expression RegulationGlucoseGlutamineHumansHypoxia-Inducible Factor 1MAP Kinase Signaling SystemNeoplasmsNitrogenOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAdenosine TriphosphateBiomarkers, TumorCarbonGlucoseGlutamineHypoxia-Inducible Factor 1NitrogenOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-myc

Identifiers

PMID22339657
PMCPMC4505802
OpenAlexW2060150859

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.