Panoply™ Human HLA-G Knockdown Stable Cell Line

Name: Panoply™ Human HLA-G Knockdown Stable Cell Line
SKU: CSC-DC007104
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-DC007104

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Gene Information

Cat. No.	CSC-DC007104
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	HLA-G
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

Mycoplasma	Negative
Format	One frozen vial containing millions of cells
Storage	Liquid nitrogen
Safety Considerations	The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship	Dry ice

Gene Name	HLA-G major histocompatibility complex, class I, G [ Homo sapiens ]
Gene Symbol	HLA-G
Synonyms	HLA-G; major histocompatibility complex, class I, G; HLA G histocompatibility antigen, class I, G; HLA class I histocompatibility antigen, alpha chain G; b2 microglobulin; HLA G antigen; HLA class I molecule; MHC class I antigen G; HLA-G histocompatibility antigen, class I, G; MHC-G;
GeneID	3135
Uni ProtID	P17693
mRNA Refseq	BC021708
Chromosome Location	6p21.3
Function	MHC class I receptor activity; protein homodimerization activity; receptor binding;
Pathway	Adaptive Immune System, organism-specific biosystem; Allograft rejection, organism-specific biosystem; Allograft rejection, conserved biosystem; Antigen Presentation: Folding, assembly and peptide loading of class I MHC, organism-specific biosystem; Antigen processing and presentation, organism-specific biosystem; Antigen processing and presentation, conserved biosystem; Antigen processing-Cross presentation, organism-specific biosystem;
MIM	142871

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Immunotherapy for solid tumors has long been hampered by the development of an immunosuppressive tumor microenvironment and the lack of specific tumor-associated antigens that can be targeted across diverse solid tumor types. Human leukocyte antigen G (HLA-G), an immune checkpoint protein (ICP), is newly expressed on most tumor cells as a means of evading immune attack and has recently been demonstrated in vitro as a useful target for chimeric antigen receptor (CAR)-T therapy for leukemia. Here, researchers developed a novel CAR strategy using natural killer (NK) cells as effector cells, characterized by enhanced cytolysis through DAP12-based intracellular signaling. Results showed that HLA-G CAR-transduced NK cells exhibited potent cytolysis against breast, brain, pancreatic, and ovarian cancer cells in vitro and inhibited xenograft tumor growth and prolonged median survival in orthotopic mouse models. In tumor co-culture experiments, the anti-HLA-G scFv portion promoted Syk/Zap70 activation in NK cells, suggesting a potential reversal of HLA-G-mediated immunosuppression, thereby restoring the cytolytic function of natural NK cells. Low-dose chemotherapy further induced tumor HLA-G expression, and combined with anti-HLA-G CAR-NK therapy, it achieved extensive tumor ablation in vitro and in vivo. Tumor HLA-G upregulation involves inhibition of DNMT1 and demethylation of the transporter associated with antigen processing 1 promoter.

Here, researchers tested the antitumor activity of HLA-G CAR-NK cells using MDA-MB-231, DBTRG-05MG, AsPC-1, and SKOV3 cells as in vitro models. At the same E:T ratio, with increasing time and NK cell titers, anti-HLA-G CAR-NK cells exhibited enhanced cytotoxicity compared to parental control NK cells (Figure 1D). Using stably HLA-G knockdown MDA-MB-231 and AsPC-1 cells, researchers confirmed that the enhanced killing capacity of HLA-G CAR-NK cells was dependent on HLA-G expression, and these HLA-G knockdown cells were more sensitive to parental NK cell-mediated cytotoxicity (Figure 1E). Taken together, these results demonstrate that HLA-G CARs can enhance NK cell cytotoxicity against a variety of solid tumor cells and that this cytotoxicity is HLA-G dependent.

Figure 1. Cytotoxic killing of multiple solid tumor cell lines by anti-HLA-G CAR-NK cells. (Jan C I, et al., 2021)

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