CCL5 Target Analysis Report Summary
About the Target
Based on the provided context information, the key viewpoints regarding CCL5 can be summarized as follows:
CCL5 plays a role in recruiting mesenchymal stem cells (MSCs) to the site of breast tumors, promoting their secretion of CXCL10 and CCL5, which enhance the metastatic potential of breast cancer cells (BCCs). Additionally, CCL5 stimulates BCCs and stromal cells to secrete matrix metalloproteinases (MMPs), facilitating the breakdown of the extracellular matrix and further promoting BCC metastasis [1].
In the context of glioblastoma (GBM), CCL5-CCR5 signaling contributes to cancer progression and the homing of cancer stem cells to their niche. Both GBM cells and stromal cells express CCL5 and its receptor CCR5, leading to mutual activation and stimulation in a paracrine signaling manner. This interaction influences local immunity modulation and attracts effector cells [2].
The release of CCL5, along with other cyto/chemokines, is associated with inflammatory and tolerogenic activities at the maternal-fetal interface during placental development. However, AMA peptides negatively impact this process, affecting cellular homeostasis and causing dysregulation of cellular outcomes [3].
Radiation exposure leads to the activation of various molecular effects involving CCL5, such as the upregulation of CCL5 and CCL2 to attract T cell infiltration in the tumor microenvironment. Additionally, radiation-generated dsDNA fragments activate the STING pathway to induce T cell activation [4].
In the context of rheumatoid arthritis (RA), BMP (Bone Morphogenetic Protein) signaling and CCL5 are involved in the pathogenesis of the disease. BMP production appears to have an anti-inflammatory role under normal conditions, downregulating pro-inflammatory cytokines and chemokines. However, in the presence of increased levels of pro-inflammatory factors like TNF-alpha and IL-17, synoviocytes become activated and produce higher levels of BMPs. This, in turn, contributes to the recruitment and activation of immune cells, along with increased levels of pro-inflammatory factors, contributing to RA [5].
Overall, CCL5 is involved in various biological processes related to cancer progression, immune modulation, placental development, radiation-induced effects, and rheumatoid arthritis pathogenesis.
Figure [1]
Figure [2]
Figure [3]
Figure [4]
Figure [5]
Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the CCL5 target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
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