The tumor microenvironment (TME) is composed of tumor cells and various interstitial cells and extracellular matrices, including fibroblasts, endothelium, immunocytes, mesenchymal stem cell, etc. Cancer-associated fibroblasts (CAFs) are the most abundant mesenchymal cells in TME, which are activated fibroblasts. CAFs have functional heterogeneity, which can promote or inhibit the growth of cancer. Studies have shown that CAFs promote tumor proliferation, metastasis, angiogenesis, drug resistance, immune escape, and ECM remodeling.
CAFs can form complex molecular networks and exert their biological functions when they interact with immune cells and tumor cells through various signal pathways, such as autocrine and paracrine. The interaction between CAFs and tumor cells is complementary. Under certain conditions, CAFs can induce the origin of tumor and the proliferation of tumor cells, and tumor cells can also promote the generation and activation of CAFs. CAFs secrete many cell growth factors, such as FGF and SDF-1/CXCL12, which promote the growth and proliferation of tumor cells. Tumor cells secrete cytokines to promote CAFs formation and aggregation, which contributes to tumor invasion and metastasis. CAFs also secrete various cytokines and chemokines that act on various immune cells, such as cytotoxic T lymphocytes, regulatory T cells (Tregs), and macrophages, coordinate the immunosuppressive microenvironment, resulting in immune escape. In addition, activated immune cells secrete cytokines, that induce the conversion of normal fibroblasts into inflammatory CAFs, further promoting the recruitment of immunosuppressive cells and immunosuppression in TME.
The tumor-promoting function of CAFs in the development of cancer makes it a promising therapeutic target in cancer therapy. However, the interaction of CAFs with tumor cells and immune cells is complex, and the key effector molecules regulating tumor immunity should be further explored, the key problem to be solved in the future is to find specific molecular markers or to explore the biological functions of different subtypes. For this research topic, we would like to create a special subject to introduce the latest advances in the mechanisms of fibroblast-tumor cell interaction and target selection. We welcome original research articles and comments dedicated to:
• The mechanism of fibroblasts regulating tumor cells in the immune microenvironment.
• Screening and verification of targets related to mutual editing between fibroblasts and tumor cells.
• Function and classification of cancer-associated fibroblasts regulated by tumor cells.
• Therapeutic strategies for targeting cancer-associated fibroblasts to enhance the anti-cancer immune response.
• Exploration of biomarkers and therapeutic targets related to cancer-associated fibroblasts.
The tumor microenvironment (TME) is composed of tumor cells and various interstitial cells and extracellular matrices, including fibroblasts, endothelium, immunocytes, mesenchymal stem cell, etc. Cancer-associated fibroblasts (CAFs) are the most abundant mesenchymal cells in TME, which are activated fibroblasts. CAFs have functional heterogeneity, which can promote or inhibit the growth of cancer. Studies have shown that CAFs promote tumor proliferation, metastasis, angiogenesis, drug resistance, immune escape, and ECM remodeling.
CAFs can form complex molecular networks and exert their biological functions when they interact with immune cells and tumor cells through various signal pathways, such as autocrine and paracrine. The interaction between CAFs and tumor cells is complementary. Under certain conditions, CAFs can induce the origin of tumor and the proliferation of tumor cells, and tumor cells can also promote the generation and activation of CAFs. CAFs secrete many cell growth factors, such as FGF and SDF-1/CXCL12, which promote the growth and proliferation of tumor cells. Tumor cells secrete cytokines to promote CAFs formation and aggregation, which contributes to tumor invasion and metastasis. CAFs also secrete various cytokines and chemokines that act on various immune cells, such as cytotoxic T lymphocytes, regulatory T cells (Tregs), and macrophages, coordinate the immunosuppressive microenvironment, resulting in immune escape. In addition, activated immune cells secrete cytokines, that induce the conversion of normal fibroblasts into inflammatory CAFs, further promoting the recruitment of immunosuppressive cells and immunosuppression in TME.
The tumor-promoting function of CAFs in the development of cancer makes it a promising therapeutic target in cancer therapy. However, the interaction of CAFs with tumor cells and immune cells is complex, and the key effector molecules regulating tumor immunity should be further explored, the key problem to be solved in the future is to find specific molecular markers or to explore the biological functions of different subtypes. For this research topic, we would like to create a special subject to introduce the latest advances in the mechanisms of fibroblast-tumor cell interaction and target selection. We welcome original research articles and comments dedicated to:
• The mechanism of fibroblasts regulating tumor cells in the immune microenvironment.
• Screening and verification of targets related to mutual editing between fibroblasts and tumor cells.
• Function and classification of cancer-associated fibroblasts regulated by tumor cells.
• Therapeutic strategies for targeting cancer-associated fibroblasts to enhance the anti-cancer immune response.
• Exploration of biomarkers and therapeutic targets related to cancer-associated fibroblasts.