The Complement System in Ovarian Cancer: An Underexplored Old Path
Related Experiment Video
Updated: Oct 25, 2025
Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1
Published on: December 5, 2020
Yaiza Senent1,2,3, Daniel Ajona1,2,3,4, Antonio González-Martín1,5
1Translational Oncology Group, Program in Solid Tumors, Cima University of Navarra, 31008 Pamplona, Spain.
Abstract:
Ovarian cancer is one of the most lethal gynecological cancers. Current therapeutic strategies allow temporary control of the disease, but most patients develop resistance to treatment. Moreover, although successful in a range of solid tumors, immunotherapy has yielded only modest results in ovarian cancer. Emerging evidence underscores the relevance of the components of innate and adaptive immunity in ovarian cancer progression and response to treatment. Particularly, over the last decade, the complement system, a pillar of innate immunity, has emerged as a major regulator of the tumor microenvironment in cancer immunity. Tumor-associated complement activation may support chronic inflammation, promote an immunosuppressive microenvironment, induce angiogenesis, and activate cancer-related signaling pathways. Recent insights suggest an important role of complement effectors, such as C1q or anaphylatoxins C3a and C5a, and their receptors C3aR and C5aR1 in ovarian cancer progression. Nevertheless, the implication of these factors in different clinical contexts is still poorly understood. Detailed knowledge of the interplay between ovarian cancer cells and complement is required to develop new immunotherapy combinations and biomarkers. In this context, we discuss the possibility of targeting complement to overcome some of the hurdles encountered in the treatment of ovarian cancer.
Insights
The complement system, part of innate immunity, significantly influences ovarian cancer progression and treatment resistance. Targeting complement may offer new therapeutic strategies for this lethal gynecological cancer.
Area of Science:
- Immunology
- Oncology
- Gynecologic Oncology
Background:
- Ovarian cancer remains a leading cause of cancer death among women.
- Current treatments often lead to therapy resistance, limiting long-term patient survival.
- Immunotherapy shows limited efficacy in ovarian cancer, necessitating novel therapeutic approaches.
Purpose of the Study:
- To explore the role of the complement system in ovarian cancer immunity.
- To understand how complement activation impacts the tumor microenvironment and disease progression.
- To discuss the potential of targeting complement pathways for improved ovarian cancer treatment.
Main Methods:
- Review of current literature on innate and adaptive immunity in ovarian cancer.
- Analysis of the complement system's components (e.g., C1q, C3a, C5a) and their receptors (C3aR, C5aR1).
- Discussion of complement's role in inflammation, immunosuppression, angiogenesis, and signaling pathways within the tumor microenvironment.
Main Results:
- Complement activation within the tumor microenvironment can promote chronic inflammation and immunosuppression.
- Complement effectors like C1q, C3a, and C5a are implicated in ovarian cancer progression.
- The precise clinical implications of these complement factors require further investigation.
Conclusions:
- The complement system is a critical regulator of ovarian cancer immunity and progression.
- Understanding the interplay between ovarian cancer cells and complement is crucial for developing new therapies.
- Targeting the complement system presents a promising strategy to overcome treatment resistance and improve outcomes in ovarian cancer.
Related Concept Videos
01:27Complement System
02:53Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
01:30Hormonal Control of the Ovarian Cycle
Before puberty, the hypothalamus releases GnRH in a low frequency, low amplitude pulsatile manner. This along with the immature hypothalamic-pituitary-gonadal axis activity, results in low estrogen levels and the absence of a fully functional ovarian cycle. At puberty, GnRH secretion increases in both frequency and...
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...