Evidence map›Paper›PMID 16080799›Full record

ArticleBMC cancer2005

Effects of alpha fetoprotein on escape of Bel 7402 cells from attack of lymphocytes.

Mengsen Li, Xinhua Liu, Sheng Zhou, Pingfeng Li, Gang Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

19 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Alpha-fetoprotein: Past, present, and future.Hepatology communications · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Alpha-Fetoprotein and Hepatocellular Carcinoma Immunity.Canadian journal of gastroenterology & hepatology · 2018
    Review
  11. Article
  12. Nonsecreted cytoplasmic alpha-fetoprotein: a newly discovered role in intracellular signaling and regulation. An update and commentary.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  13. Article
  14. Article
  15. Review of the adenocarcinoma cell surface receptor for human alpha-fetoprotein; proposed identification of a widespread mucin as the tumor cell receptor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Review
  16. Article
  17. Article
  18. Review
  19. 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

5 authors at 2 institutions in 1 country.

Mengsen LiDepartment of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100083, China. ligang55@263.net
Xinhua Liu
Sheng Zhou
Pingfeng Li
Gang Li
Peking University · CNHainan Medical College Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInvolvement of AFP against apoptosis of tumor cell has been implicated in its evasion of immune surveillance. However, the molecular events of immune escape mechanisms are still unknown. The major observations reported here relate to a possible mechanism by which heptoloma Bel 7402 cells escape immune surveillance in vitro.

methodsWestern blotting and a well-characterized cofocal scanning image were performed to analyze the expression of Fas/FasL and caspase-3 in co-cultured Bel 7402 and Jurkat cells.

resultsAfter co-culture with Jurkat cells, up-regulated Fas and reduced FasL expression could be observed. Treatment with AFP could remarkably inhibit the elevated Fas and, whereas, induce the FasL expression in co-cultured Bel 7402 cells. Cells co-culture could induce the expression of caspase-3 in both cells line. The elevated caspase-3 in Bel 7402 cells was abolished following the treatment of AFP. The expression of caspase-3 was elevated in co-cultured Jurkat cells treated with AFP. No detectable change on the expression of survivin was examined in both cells line. Monoclonal antibody against AFP treatment alone did not obviously influence the growth of cells, as well as the expression of Fas/FasL and caspase-3. However, the effect of AFP could be blocked by antibody.

conclusionsour results provide evidence that AFP could promote the escape of liver cancer cells from immune surveillance through blocking the caspase signal pathway of tumor cells and triggering the Fas/FasL interaction between tumor cells and lymphocytes.

Indexed as

Gene Expression Regulation, Neoplasticalpha-FetoproteinsAntibodies, MonoclonalBlotting, WesternCaspase 3CaspasesCell Line, TumorCell ProliferationCoculture TechniquesFas Ligand Proteinfas ReceptorHumansInhibitor of Apoptosis ProteinsJurkat CellsLymphocytesMembrane Glycoproteinsalpha-FetoproteinsAntibodies, MonoclonalBIRC5 protein, humanCASP3 protein, humanCaspase 3CaspasesFASLG protein, humanFas Ligand Proteinfas ReceptorInhibitor of Apoptosis ProteinsMembrane GlycoproteinsMicrotubule-Associated ProteinsNeoplasm ProteinsSurvivinTumor Necrosis Factors

Identifiers

PMID16080799
PMCPMC1198224
OpenAlexW2124418353

What OpenQuestion holds

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LicenceCC BY
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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.