This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about C-C chemokine receptor type 9.
Receptor for chemokine SCYA25/TECK.
Subsequently transduces a signal by increasing the intracellular calcium ions level..
Human | |
---|---|
Gene Name: | CCR9 |
Uniprot: | P51686 |
Entrez: | 10803 |
Belongs to: |
---|
G-protein coupled receptor 1 family |
C-C chemokine receptor type 9; C-C CKR-9; CC-CKR-9; CCR9; CCR-9; CD199; CDw199 antigen; CDw199; chemokine (C-C motif) receptor 9; G protein-coupled receptor 28; GPR28; GPR-9-6G-protein coupled receptor 28
Mass (kDA):
42.016 kDA
Human | |
---|---|
Location: | 3p21.31 |
Sequence: | 3; NC_000003.12 (45886504..45903177) |
Highly expressed in the thymus and low in lymph nodes and spleen.
Cell membrane; Multi-pass membrane protein.
What are the most effective uses of the CCR9 marker? This article discusses the role CCR9 is playing as a biomarker to detect tumors. We will talk about how CCR9 may be used to detect cancer cells and how it might be targeted with targeted treatment. We will then discuss the potential uses for CCR9 antagonists in the treatment of CCR9-overexpressed cancers.
CCR9 was identified as a cancer biomarker. It has raised the question of "What does this mean to the future of cancer immunotherapy?" CCR9 has been identified as being highly expressed in various types of cancers. This may make it a therapeutic target for cancer drugs. Further research will reveal the exact role of this biomarker for the development of new cancer therapies. This research has important implications for cancer immunotherapy and the future of cancer diagnosis.
CCR9 expression was observed to be higher in lung cancer patients who had advanced stage. CCR9 can only be expressed in certain tissues. However the interaction between CCR9 & CCL25 has been implicated with many cancer signaling pathways. CCR9 also has poor responses to anti-TNF antibody drugs. CCR9 is therefore an important biomarker in lung cancer.
Moreover, a study of non-small-cell lung cancer (NSCLC) patients showed that patients with high CCR9 expression had poor overall survival. In addition, high levels of ALDh2A1 within the tumor microenvironment were associated with higher CCR9 expression. Furthermore, CCR9-expressing CSCs were found to migrate faster in response to CCL25 stimulation, and an anti-CCR9 antibody reversed this effect.
Using a Kaplan-Meier survival analysis, we analyzed the association between CCR9 expression and OS in CCR9-positive and non-CDh2 patients. Patients with high CCR9 expressed were more likely to survive than those with lower CCR9 expression. This study's results are promising for the discovery of new tumor biomarkers.
CBIS was used to develop anti-hCCR9 antibodies. After creating stable transfectants we used these mAbs to immunize and flow cytometrically screen cells. Two mice were immunized for CHO/hCCR9, and hybridomas were seeded in 96well plates. From this, we selected CCR9-positive hybridomas and analyzed the mAb's binding activity to these cells. After limiting the dilution we identified C9Mab-1 to be an IgG1 kappa antibody.
CCR9 is a receptor located on the surface of thymocytes. It is expressed in both immature T-cells and antigen-experienced cells. It seems to be involved in T-cell maturation and presentation of antigens to T cells. The CCR9 receptor protein is also expressed on ECs in gut-associated tissues and is found in a small subset of CD4 and CD8 lymphocytes. The receptor has also been discovered in peripheral blood cells of B cells.
This study shows that CCR9 is a biomarker for early cancer. CC chemokine receptacles have many targets. CCR10 expression has a positive correlation with immune cell growth, whereas CCR9 expression can negatively correlate with neutrophil and macrophage colonization. CCR10 can be used to determine the diagnosis and treatment for LUAD.
Chemokines like CCR9 are important for the survival of cancer cells. Drugs that target CCR9 will likely have a higher therapeutic efficacy because it is widely expressed. Targeted therapies are an effective way to reduce systemic side effect of chemotherapy drugs and improve antitumor efficiency. Here are some examples for treatments that target CCR9.
CCX282-B has shown efficacy in inducing remission in active CD. In clinical trials, CCX282-B proved to be significantly more effective than placebo in maintaining remission. However, vedolizumab showed high effectiveness in studies of patients suffering from UC. Targeting CCR9 for IBD is a promising prospect because genetic targeting can relieve inflammation.
Multiple monoclonal anti-CCR9 antibodies have been developed through molecular research into the mechanisms of CCR9 antibody action. These monoclonal antibodies were chosen for their differences in epitope specificity, binding affinities, and other factors. High melting points mean greater potency and fewer side effects. Despite their differences, anti-CCR9 mAbs have proven to be effective in inducing tumor-specific cytotoxicity.
Molecular biology studies of the chemokine receptor CCR9 have revealed that it plays an important role in cancer development. Chemokines are found on both tumor and immune tissues in cancer. Their presence is associated wit poor survival. CCR9 is also linked to metastasis and invasiveness. CCR9 expression in tumors is linked to higher response rates to chemotherapy than those with non-CCR9 genes.
These trials were not conclusive. CCR9-blocking drugs have not been shown to be effective in CD. Phase IIb PROTECT-1, SHIELD-1 and Phase III studies (CCR9) showed efficacy. The SHIELD program termination resulted in the end of the unsuccessful Phase III study (CCR9). A phase III study to assess the long-term consequences of CCR9 Blockade in CD was also planned.
CCR9 expression is positively correlated in lung cancer with the presence ALDh2A1+CSCs. CCR9 expression levels were higher in ALDHhigh CSCs that in ALDh2A1+Tumorcells. These results were confirmed by real-time quantitative PCR. The CCR9/CCL25 ratio of a mouse model was increased in ALDHhigh CSCs.
Anti-CCR9 antibodies have an excellent affinity for the protein. The 92R Ab binds to the entire cDNA sequence from the hCCR9 and endogenous CCR9 proteins expressed in MOLT-4 cells. 92R and 91R are cross-competing mAbs. The 92R MAb binds to an epitope within the N-terminal region of hCCR9 This binding allows CCR9-targeted therapies for cancer cells to be made possible by this peptide.
In the past, researchers discovered that antibodies against CCR9 receptor could inhibit cell growth. Anti-bodies against CCR9 were shown to inhibit tumor growth and angiogenesis in laboratory studies. In mice, they inhibited tumor growth, reduced tumor size by 85 percent, and increased apoptotic and necrotic cells. Different types of cancer are currently undergoing clinical trials for chemokine-receptor antagonists.
Antibodies against CCR9 have also shown promising results in trials for treating IBD. They block the migration o effector T cell cells into the intestinale, which could cause inflammation in patients with inflammatorybowel disease (IBD).
A further challenge is the limited time available for the development of anti-CCR9 therapies. For example, 12 weeks may not be enough time to clear out effector populations in the lamina propria. Recruited cells may remain in the lamina propria for many weeks before dying in situ. Therefore, it is essential to conduct more trials that will determine the efficacy of CCR9-blockade therapy.
In addition to regulating T-cell differentiation, CCR9 has been shown to regulate the recruitment of T cells to the thymus. CCR9 was knocked down in mice to reduce the ratio of subgroups within T cells. Knockdown CCR9 in mice also enhanced gdT cells in their intestines and suppressed the differentiation forkhead protein 3+ regulatory cells.
The regulation of cancer cell invasion, metastasis and metastasis by chemotherapy receptors is controlled by chemokine receptors. They also regulate migration and induce epithelial-mesenchymal transition. Studies have shown a higher incidence of metastasis from CCR9-overexpressed tumors to bone marrow and lymph nodes. CXCR4, a CCR9-related gene, has been shown to be linked to metastasis to lymph nodes and bone marrow. Important for lymph node metastasis is chemokine-signaling regulation of CCL19/CCL21–CCR7.
CCR9/CCL25 chemokine receptors are required for several functions in T cell. Blocking CCR9/CCL25 signaling could inhibit induced T-cell co-stimulator (ITCg) and interleukin-21 (1 IL-21) production in cells. These pathways regulate various immune processes. Blocking their activity may also enhance the anti-inflammatory effects of CCR9 antibodies.
Antibodies that target CCR9 receptors have been shown in the past to suppress tumor growth. These agents can be applied to existing or newly formed CCR9-overexpressed cancers. Anti-CD25 monoclonal antibodies inhibit the interaction CCR1/CCL5 and have shown promising outcomes in preventing tumor growth as well as reducing Bcl-2.
Future studies that focus on CCR9 and the treatment of cancer will need to examine the signaling pathway as well as the receptor. Antibodies to CCR9 will likely provide new treatments. CCR9 receptors are involved in invasion, migration and anti-apoptotic signaling. CCR9 had never been identified in a clinical setting.
PMID: 10229797 by Zaballos A., et al. Identification of the orphan chemokine receptor GPR-9-6 as CCR9, the receptor for the chemokine TECK.
PMID: 10640743 by Yu C.-R., et al. CCR9A and CCR9B: two receptors for the chemokine CCL25/TECK/Ck beta- 15 that differ in their sensitivities to ligand.