Evidence map›Paper›PMID 24625663›Full record

ReviewInternational journal of molecular sciences2014

Sphingolipids: key regulators of apoptosis and pivotal players in cancer drug resistance.

Paola Giussani, Cristina Tringali, Laura Riboni, Paola Viani, Bruno Venerando

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  3. Review
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  8. Article
  9. Drug Resistance: The Role of Sphingolipid Metabolism.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
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  18. Reduced sulfatide content in deferoxamine-induced senescent HepG2 cells.The international journal of biochemistry & cell biology · 2023
    Article
  19. Review
  20. Article

11 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Paola GiussaniDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan 20090), Italy. paola.giussani@unimi.it.
Cristina TringaliDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan 20090), Italy. cristina.tringali@unimi.it.
Laura RiboniDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan 20090), Italy. laura.riboni@unimi.it.
Paola VianiDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan 20090), Italy. paola.viani@unimi.it.
Bruno VenerandoDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan 20090), Italy. bruno.venerando@unimi.it.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance elicited by cancer cells still constitutes a huge problem that frequently impairs the efficacy of both conventional and novel molecular therapies. Chemotherapy usually acts to induce apoptosis in cancer cells; therefore, the investigation of apoptosis control and of the mechanisms used by cancer cells to evade apoptosis could be translated in an improvement of therapies. Among many tools acquired by cancer cells to this end, the de-regulated synthesis and metabolism of sphingolipids have been well documented. Sphingolipids are known to play many structural and signalling roles in cells, as they are involved in the control of growth, survival, adhesion, and motility. In particular, in order to increase survival, cancer cells: (a) counteract the accumulation of ceramide that is endowed with pro-apoptotic potential and is induced by many drugs; (b) increase the synthesis of sphingosine-1-phosphate and glucosylceramide that are pro-survivals signals; (c) modify the synthesis and the metabolism of complex glycosphingolipids, particularly increasing the levels of modified species of gangliosides such as 9-O acetylated GD3 (αNeu5Ac(2-8)αNeu5Ac(2-3)βGal(1-4)βGlc(1-1)Cer) or N-glycolyl GM3 (αNeu5Ac (2-3)βGal(1-4)βGlc(1-1)Cer) and de-N-acetyl GM3 (NeuNH(2)βGal(1-4)βGlc(1-1)Cer) endowed with anti-apoptotic roles and of globoside Gb3 related to a higher expression of the multidrug resistance gene MDR1. In light of this evidence, the employment of chemical or genetic approaches specifically targeting sphingolipid dysregulations appears a promising tool for the improvement of current chemotherapy efficacy.

Indexed as

AnimalsAntineoplastic AgentsApoptosisDrug Resistance, NeoplasmHumansModels, BiologicalNeoplasmsSignal TransductionSphingolipidsAntineoplastic AgentsSphingolipids

Identifiers

PMID24625663
PMCPMC3975402
OpenAlexW2080220600

What OpenQuestion holds

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LicenceCC BY
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.