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Related Concept Videos

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

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Related Experiment Video

Updated: Jun 8, 2026

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
06:54

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

Cancer and the complement cascade.

Martin J Rutkowski1, Michael E Sughrue, Ari J Kane

  • 1Department of Neurological Surgery, University of California at San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143, USA.

Molecular Cancer Research : MCR
|September 28, 2010
PubMed
Summary
This summary is machine-generated.

The complement cascade, a part of innate immunity, may surprisingly promote cancer development. This review explores how complement proteins drive key cancer features like proliferation and immune evasion.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Inflammation and immunosurveillance are well-studied in tumors.
  • The oncogenic role of the complement cascade in cancer remains under-explored.
  • Emerging evidence suggests complement proteins may contribute to tumor growth and regeneration.

Purpose of the Study:

  • To investigate the hypothesis that complement proteins promote carcinogenesis.
  • To elucidate mechanisms by which complement drives fundamental cancer features.
  • To re-evaluate the role of complement in neoplasia beyond its traditional immune functions.

Main Methods:

  • Review of existing literature on complement system functions.
  • Analysis of evidence linking complement proteins to cancer hallmarks.
  • Exploration of proposed molecular mechanisms.

Main Results:

  • Complement proteins facilitate dysregulation of mitogenic signaling pathways.
  • Evidence indicates complement promotes sustained cellular proliferation and angiogenesis.
  • Complement aids in insensitivity to apoptosis, invasion, migration, and immune evasion.

Conclusions:

  • The complement cascade may act as an oncogenic driver, contrary to its role in cancer defense.
  • Complement proteins can promote fundamental cancer characteristics, suggesting a dual role in neoplasia.
  • A paradigm shift is needed to consider complement's contribution to cancer development.