Evidence map›Paper›PMID 33646427›Full record

ReviewAmino acids2021

Reprogramming of mitochondrial proline metabolism promotes liver tumorigenesis.

Zhaobing Ding, Russell E Ericksen, Qian Yi Lee, Weiping Han

Abstract readReview
PubMed Publisher
In one paragraph

Review in Amino acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. [Research Progress on the Role and Mechanisms of PYCR1 
in Tumorigenesis and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  5. Review
  6. Review
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. Characteristics ofHeliyon · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Novel Fragment Inhibitors of PYCR1 from Docking-Guided X-ray Crystallography.Journal of chemical information and modeling · 2024
    Article
  17. Review
  18. Glutamine metabolic reprogramming in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023
    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

4 authors at 1 institution in 2 countries.

Zhaobing DingInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), #02-02 Helios, 11 Biopolis Way, Singapore, 138667, Singapore.
Russell E EricksenInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), #02-02 Helios, 11 Biopolis Way, Singapore, 138667, Singapore.
Qian Yi LeeInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), #02-02 Helios, 11 Biopolis Way, Singapore, 138667, Singapore.
Weiping HanInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), #02-02 Helios, 11 Biopolis Way, Singapore, 138667, Singapore. wh10@cornell.edu.ORCID http://orcid.org/0000-0002-5023-2104
Agency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated cellular energetics has recently been recognized as a hallmark of cancer and garnered attention as a potential targeting strategy for cancer therapeutics. Cancer cells reprogram metabolic activities to meet bio-energetic, biosynthetic and redox requirements needed to sustain indefinite proliferation. In many cases, metabolic reprogramming is the result of complex interactions between genetic alterations in well-known oncogenes and tumor suppressors and epigenetic changes. While the metabolism of the two most abundant nutrients, glucose and glutamine, is reprogrammed in a wide range of cancers, accumulating evidence demonstrates that additional metabolic pathways are also critical for cell survival and growth. Proline metabolism is one such metabolic pathway that promotes tumorigenesis in multiple cancer types, including liver cancer, which is the fourth main cause of cancer mortality in the world. Despite the recent spate of approved treatments, including targeted therapy and combined immunotherapies, there has been no significant gain in clinical benefits in the majority of liver cancer patients. Thus, exploring novel therapeutic strategies and identifying new molecular targets remains a top priority for liver cancer. Two of the enzymes in the proline biosynthetic pathway, pyrroline-5-carboxylate reductase (PYCR1) and Aldehyde Dehydrogenase 18 Family Member A1 (ALDH18A1), are upregulated in liver cancer of both human and animal models, while proline catabolic enzymes, such as proline dehydrogenase (PRODH) are downregulated. Here we review the latest evidence linking proline metabolism to liver and other cancers and potential mechanisms of action for the proline pathway in cancer development.

Indexed as

AnimalsCarcinogenesisCellular ReprogrammingHumansLiverLiver NeoplasmsMitochondriaProlineProlineCancerEnzymeHepatocellular carcinomaMetabolismProline

Identifiers

PMID33646427
OpenAlexW3134784280

What OpenQuestion holds

Textmetadata
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.