mProX™ Human CCR8 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human CCR8 Stable Cell Line (S01YF-0923-PY41). Click the button above to contact us or submit your feedback about this product.
Michelle (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Christopher (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 CCR8 plays an essential role in facilitating the migration and invasion of breast cancer cells through its interaction with the chemokine CCL18.
In a 24-hour treatment, 5637 bladder cancer cells underwent exposure to CCL18 (50 ng/ml), CCL18 combined with NT shRNA, or CCL18 combined with CCR8 shRNA. Assessments of invasion (via Transwell assays, A and B) and migration (through wound healing assays, C and D) were conducted, each observed at a ×100 magnification. Statistically significant differences were noted (*P<0.05) compared to the NC group, while (**P<0.05) contrasts were identified in comparison to the CCL18 + NT shRNA group. Notations: CCL18, chemokine (C-C motif) ligand 18; CCR8, chemokine (C-C motif) receptor 8; NC, normal control; NT, non-target; shRNA, short hairpin RNA.
Ref: Liu, Xiaoqiang, et al. "CCL18 enhances migration, invasion and EMT by binding CCR8 in bladder cancer cells." Molecular medicine reports 19.3 (2019): 1678-1686.
Pubmed: 30592282
DOI: 10.3892/mmr.2018.9791
Research Highlights
Sun T, et al. "Oxamate enhances the efficacy of CAR-T therapy against glioblastoma via ." Journal of experimental & clinical cancer research : CR, 2023.
Chimeric antigen receptor (CAR)-T immunotherapy has shown limited success in treating solid tumors. One contributing factor is the immunosuppressive microenvironment created by excess lactate produced by tumor glycolysis. However, the specific mechanism by which lactate induces immunosuppression remains unclear. In this study, the researchers used flow cytometry and immunohistochemical staining to analyze immunocyte subpopulations and molecular characteristics in orthotopic xenografts of nude mice. They found that treatment with oxamate, a lactate dehydrogenase A inhibitor, in combination with T or CAR-T cell injection, promoted immune activation of tumor-infiltrating CAR-T cells and increased infiltration of regulatory T cells in a glioblastoma mouse model. Further experiments revealed that lactate upregulated the expression of specific immune molecules in both lactate-treated cells and glioma stem cell-co-cultured CD4+ T cells and macrophages. This effect was mediated through histone H3K18 lactylation. These findings suggest that inhibiting lactate production may be a potential strategy for enhancing CAR-T function in glioblastoma therapy.
Pubmed:
37770937
DOI:
10.1186/s13046-023-02815-w
Chu YT, et al. "Interplay of Chemokines Receptors, Toll-like Receptors, and Host Immunological ." Biomedicines, 2023.
The study investigated the correlation between different chemokine receptors and specific T helper (TH) cell responses. Results showed that CCR5 was associated with TH1 responses, CCR1 with TH1-like responses, CCR4 with TH2 and TH9 responses in basophils, CCR3 with TH2 and TH9 responses in eosinophils, CCR10 with TH22 responses, CCR6 with TH17 responses, CXCR3 with THalphabeta responses, CCR8 with regulatory T cells (Treg), and CCR2 with TH3 responses. This information is significant in identifying biomarkers for different immune cells and understanding the underlying mechanisms of immune pathways. Adequate understanding of the chemokine and Toll-like receptor system is crucial for comprehending the function of both innate and adaptive immune responses.
Pubmed:
37760825
DOI:
10.3390/biomedicines11092384