mProX™ Human CXCR6 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 CXCR6 overexpression promotes invasion and migration in gastric cancer cells.
Elevated CXCR6 expression markedly enhanced both invasiveness and migratory capacity in HGC-27 cells, with statistical significance represented as ***P<0.001 and ****P<0.0001. Visual examination at 40x magnification confirmed these findings.
Ref: Jin, Jie-Jie, et al. "CXCR6 predicts poor prognosis in gastric cancer and promotes tumor metastasis through epithelial-mesenchymal transition." Oncology reports 37.6 (2017): 3279-3286.
Pubmed: 28440473
DOI: 10.3892/or.2017.5598
Research Highlights
Uvarova AN, et al. "rs71327024 Associated with COVID-19 Hospitalization Reduces CXCR6 Promoter ." International journal of molecular sciences, 2023.
The single-nucleotide polymorphism rs71327024, located within the human 3p21.31 locus, has been linked to an increased likelihood of hospitalization after SARS-CoV-2 infection. This locus contains genes responsible for chemokine receptors that could play a role in severe COVID-19. One such gene, CXCR6, is highly expressed in T lymphocytes, NK, and NKT cells and is known to recruit immune cells in chronic inflammatory and respiratory diseases. Our research reveals that rs71327024 is located in an active enhancer that boosts the CXCR6 promoter's activity in human CD4(+) T lymphocytes. The common rs71327024(G) variant facilitates binding of the c-Myb transcription factor, while the risk rs71327024(T) variant weakens this binding and diminishes enhancer activity. This observation is supported by our findings in PMA-treated Jurkat cells with reduced c-Myb expression, which showed that the effect of rs71327024 on CXCR6 promoter activity is allele-specific. In conclusion, the presence of the risk rs71327024(T) variant could decrease CXCR6 expression in T helper cells and potentially contribute to the development of severe COVID-19 and other inflammatory conditions through the disruption of c-Myb binding.
Pubmed:
37762093
DOI:
10.3390/ijms241813790
Korbecki J, et al. "The Role of CXCR1, CXCR2, CXCR3, CXCR5, and CXCR6 Ligands in Molecular Cancer ." Cancers, 2023.
Acute myeloid leukemia (AML) is a form of leukemia characterized by poor prognoses, which has led to extensive research efforts aimed at identifying new therapeutic targets. One area of investigation is the role of extracellular factors, namely CXC chemokines, in AML. While CXCL12 (SDF-1) and its receptor CXCR4 have been extensively studied, there is a lack of research on other CXC chemokine axes in AML. The purpose of this study is to fill this gap by providing an overview of the significance of all CXC chemokines, except CXCL12, in AML's oncogenic processes. Specifically, the focus is on how CXCL1 (Gro-alpha), CXCL8 (IL-8), CXCL10 (IP-10), and CXCL11 (I-TAC), as well as CXCR1, CXCR2, CXCR3, CXCR5, and CXCR6 ligands and CXCL14 and CXCL17, impact AML tumor processes, such as cell proliferation, bone marrow angiogenesis, interactions with non-leukemic cells, and their clinical significance. The study delves into how these chemokines influence prognosis, their association with extramedullary AML, induction of chemoresistance, effects on bone marrow microvessel density, and their connection to French-American-British (FAB) classification and FLT3 gene mutations.
Pubmed:
37760523
DOI:
10.3390/cancers15184555