mProX™ Human IL4R Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Immune Checkpoint Cell Lines
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Patrick Liam (Creative Biolabs Scientific Support)
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Published Data
Fig.1 Metastatic tumor growth is influenced by survival and proliferation, which are associated with IL4Rα.
Significant reduction in tumor seeding capability was observed in both the lung and liver when R221a IL4Rα knockdown clones were compared with sh-control clones. Similarly, in the lung, 4T1 IL4Rα knockdown clones exhibited a decrease in seeding ability compared with sh-controls, while in the liver, no significant reduction in seeding ability was observed.
Ref: Venmar, Katherine T., et al. "IL4 receptor ILR4α regulates metastatic colonization by mammary tumors through multiple signaling pathways." Cancer research 74.16 (2014): 4329-4340.
Pubmed: 24947041
DOI: 10.1158/0008-5472.CAN-14-0093
Research Highlights
Zhou, Ying. et al. "Co-expression of IL-4/IL-15-based inverted cytokine receptor in CAR-T cells overcomes IL-4 signaling in immunosuppressive pancreatic tumor microenvironment." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
The efficacy of CAR-T cell therapy has been impeded by intrinsic factors within the tumor microenvironment. Strategies are being implemented to overcome these barriers and enhance the effectiveness of immunotherapies. Tumor cells release interleukin (IL)-4, which can suppress T cell function by binding to the IL-4 receptor found on their surface. To counteract IL-4-induced immunosuppression, a novel inverted cytokine receptor (ICR) was developed. This novel CAR construct, known as 4/15NKG2D-CAR, features an NKG2D-based chimeric antigen receptor that co-expresses IL-4R as an extracellular domain and IL-15R as a transmembrane and intracellular domain. By converting IL-4R inhibitory signals into IL-15R activation signals downstream, the efficacy of NKG2D-CAR-T cells was enhanced in vitro and in vivo within the pancreatic tumor microenvironment. Specifically, 4/15NKG2D-CAR-T cells displayed heightened activation, degranulation, cytokine release, and cytotoxicity against IL-4-expressing pancreatic tumor cells.
Zhou, Ying. et al. "Co-expression of IL-4/IL-15-based inverted cytokine receptor in CAR-T cells overcomes IL-4 signaling in immunosuppressive pancreatic tumor microenvironment." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023.
Pubmed:
37865999
DOI:
10.1016/j.biopha.2023.115740
Beckstead, Jacob. et al. "Asthma is associated with a lower incidence of metastatic colorectal cancer in a US patient cohort." Frontiers in oncology, 2023.
In previous pre-clinical studies, the contribution of interleukin 4 receptor (IL4R) signaling in the progression and metastasis of colorectal cancer (CRC) was examined. It was found that aberrant activation of this receptor can result in atopic diseases such as asthma. It was hypothesized that there may be a link between excessive IL4R and CRC progression, specifically in chronic asthma patients. To test this hypothesis, the Synthetic Derivative resource at Vanderbilt University Medical Center was utilized to analyze de-identified data taken from electronic medical records. The retrospective cohorts of invasive CRC patients and cancer-free equivalents were compared. Surprisingly, results showed that significantly fewer asthmatic patients developed metastatic CRC compared to non-asthmatic patients (P=0.0381). Further analysis with a larger group of 1197 cancer-free patients also showed a lower incidence of invasive CRC in asthmatics (P<0.0001). Although these findings contradicted the initial hypothesis, they suggest a potential relationship between chronic asthma and reducing the risk of metastatic CRC. This presents an intriguing possibility for future research, specifically investigating whether treatment for chronic asthma may play a role in preventing metastatic cancer.
Beckstead, Jacob. et al. "Asthma is associated with a lower incidence of metastatic colorectal cancer in a US patient cohort." Frontiers in oncology, 2023.
Pubmed:
37860183
DOI:
10.3389/fonc.2023.1253660