Evidence map›Paper›PMID 27226542›Full record

ArticleThe Journal of biological chemistry2016

Complement Membrane Attack and Tumorigenesis: A SYSTEMS BIOLOGY APPROACH.

Laurence D Towner, Richard A Wheat, Timothy R Hughes, B Paul Morgan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Complement system in tumor growth and metastases.British journal of cancer · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Inside-Out of Complement in Cancer.Frontiers in immunology · 2022
    Review
  11. Complement and Cancer-A Dysfunctional Relationship?Antibodies (Basel, Switzerland) · 2020
    Review
  12. Review
  13. Article
  14. Role of C5b-9 and RGC-32 in Cancer.Frontiers in immunology · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Complementing Cancer Metastasis.Frontiers in immunology · 2018
    Review
  20. 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 1 institution in 1 country.

Laurence D TownerFrom the Complement Biology Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, Wales, United Kingdom.
Richard A WheatFrom the Complement Biology Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, Wales, United Kingdom.
Timothy R HughesFrom the Complement Biology Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, Wales, United Kingdom.
B Paul MorganFrom the Complement Biology Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, Wales, United Kingdom MorganBP@cardiff.ac.uk.
Cardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor development driven by inflammation is now an established phenomenon, but the role that complement plays remains uncertain. Recent evidence has suggested that various components of the complement (C) cascade may influence tumor development in disparate ways; however, little attention has been paid to that of the membrane attack complex (MAC). This is despite abundant evidence documenting the effects of this complex on cell behavior, including cell activation, protection from/induction of apoptosis, release of inflammatory cytokines, growth factors, and ECM components and regulators, and the triggering of the NLRP3 inflammasome. Here we present a novel approach to this issue by using global gene expression studies in conjunction with a systems biology analysis. Using network analysis of MAC-responsive expression changes, we demonstrate a cluster of co-regulated genes known to have impact in the extracellular space and on the supporting stroma and with well characterized tumor-promoting roles. Network analysis highlighted the central role for EGF receptor activation in mediating the observed responses to MAC exposure. Overall, the study sheds light on the mechanisms by which sublytic MAC causes tumor cell responses and exposes a gene expression signature that implicates MAC as a driver of tumor progression. These findings have implications for understanding of the roles of complement and the MAC in tumor development and progression, which in turn will inform future therapeutic strategies in cancer.

Indexed as

AlgorithmsAnimalsCarcinogenesisCell Line, TumorCell Transformation, NeoplasticComplement Membrane Attack ComplexGene Expression ProfilingGene Regulatory NetworksHumansModels, ImmunologicalReal-Time Polymerase Chain ReactionSystems BiologyComplement Membrane Attack Complexcancercomplementinflammationsystems biologytumor metastasis

Identifiers

PMID27226542
PMCPMC4946912
OpenAlexW2404394227

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.