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Updated: Jul 1, 2025
A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
Cancer‑associated fibroblasts under therapy‑induced senescence in the tumor microenvironment (Review)
Qiuhua Zhang1, Yijie Lou1, Hao Fang1
1Department of Oncology, First Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.
Abstract:
Current cancer treatments target tumor cells; however, the tumor microenvironment (TME) induces therapeutic resistance, tumor development and metastasis, thus rendering these treatments ineffective. Research on the TME has therefore concentrated on nonmalignant cells. Cancer-associated fibroblasts (CAFs) are a major TME component, which contribute to cancer progression due to their diverse origins, phenotypes and functions, including cancer cell invasion and migration, extracellular matrix remodeling, tumor metabolism modulation and therapeutic resistance. Standard cancer treatment typically exacerbates the senescence-associated secretory phenotype (SASP) of senescent cancer cells and nonmalignant cells that actively leak proinflammatory signals in the TME. Therapy-induced senescence may impair cancer cell activity and compromise treatment responsiveness. CAFs and SASP are well-studied in the formation and progression of cancer. The present review discusses the current data on CAF senescence caused by anticancer treatment and assesses how senescence-like CAFs affect tumor formation. The development of senolytic medication for aging stromal cells is also highlighted. Combining cancer therapies with senolytics may boost therapeutic effects and provide novel possibilities for research.
Insights
Cancer-associated fibroblasts (CAFs) can become senescent due to cancer treatments, promoting tumor growth. Targeting these senescent CAFs with senolytics may enhance cancer therapy effectiveness.
Area of Science:
- Oncology
- Cell Biology
- Cancer Research
Background:
- The tumor microenvironment (TME) significantly influences cancer progression and therapeutic resistance.
- Cancer-associated fibroblasts (CAFs) are key cellular components within the TME, driving cancer cell invasion, metastasis, and treatment failure.
- Standard cancer therapies can induce senescence in both cancer cells and stromal cells, leading to a pro-inflammatory senescence-associated secretory phenotype (SASP).
Purpose of the Study:
- To review current data on cancer treatment-induced senescence in CAFs.
- To assess the impact of senescent CAFs on tumor formation and progression.
- To explore the potential of senolytic therapies targeting CAFs for improved cancer treatment outcomes.
Main Methods:
- Literature review of existing research on CAFs, senescence, and the TME.
- Analysis of data linking anticancer treatments to CAF senescence.
- Evaluation of the role of senescent CAFs in tumor development and response to therapy.
Main Results:
- Anticancer treatments can induce a senescence-like state in CAFs.
- Senescence-like CAFs contribute to tumor progression through various mechanisms.
- Senescent CAFs and their SASP are implicated in therapeutic resistance and metastasis.
Conclusions:
- Senescence in CAFs is a critical factor in cancer progression and treatment resistance.
- Targeting senescent CAFs with senolytic drugs presents a promising therapeutic strategy.
- Combining senolytics with conventional cancer therapies may enhance treatment efficacy and offer new research avenues.
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