Evidence map›Paper›PMID 22774984›Full record

ArticleClinical and experimental immunology2012

Sublytic complement protects prostate cancer cells from tumour necrosis factor-α-induced cell death.

L Liu, W Li, Z Li, M Kirschfink

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Complement system in tumor growth and metastases.British journal of cancer · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Review
  9. Role of C5b-9 and RGC-32 in Cancer.Frontiers in immunology · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The role of complement in tumor growth.Advances in experimental medicine and biology · 2014
    Review
  15. Review
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 2 institutions in 2 countries.

L LiuDivision of Nephrology, Department of Internal Medicine, Tongji Hospital, Wuhan, China.
W Li
Z Li
M Kirschfink
Heidelberg University · DEHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a critical component of tumour progression. Although complement and tumour necrosis factor (TNF)-α potentially exert significant anti-tumour effects, both mediators may also promote tumour progression. It has been demonstrated that sublytic complement confers resistance on tumour cells not only against lytic complement, but also other danger molecules such as perforin. In low concentrations, TNF promotes survival of malignant cells rather than exerting cytotoxic activity. In this study, we tested if sublytic complement is able to interfere with TNF-mediated tumour cell killing. Our results demonstrate that either subcytotoxic concentrations of TNF or sublytic complement rescue prostate carcinoma cells (DU145) from TNF-α-mediated cell death. Upon pretreatment with low-dose TNF-α, but not upon pre-exposure to sublytic complement, TNF resistance was associated with the down-regulation of TNF receptor 1 (TNF-R1) expression. Complement-induced protection against TNF-mediated apoptosis accompanied the induction of anti-apoptotic proteins [B cell leukaemia/lymphoma (Bcl)-2 and Bcl-xL] at an early stage followed by inhibition of the TNF-induced decrease in the amount of Bcl-2 and Bcl-xL. Cell protection also accompanied the inhibition of caspase-8 activation, poly (ADP-ribose) polymerase (PARP)-1 cleavage and the activation of nuclear factor (NF)-κB. Our data extend our current view on the induction of tumour cell resistance against cytotoxic mediators supporting the role of the tumour microenvironment in mediating protection against the anti-cancer immune response.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCaspase 8Cell DeathCell Line, TumorComplement System ProteinsCytotoxicity, ImmunologicEnzyme ActivationHumansMaleNF-kappa BPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProstatic NeoplasmsReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaApoptosis Regulatory ProteinsCaspase 8Complement System ProteinsNF-kappa BPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID22774984
PMCPMC3406369
OpenAlexW1511910965

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.